24016 Federal Register / Vol. 72, No. 83 / Tuesday, May 1, 2007 / Proposed Rules 

ENVIRONMENTAL PROTECTION 

AGENCY 

40 CFR Part 141 

[EPA–HQ–OW–2007–0068 FRL–8301–3] 

RIN 2040–AE58 

Drinking Water: Regulatory 

Determinations Regarding 

Contaminants on the Second Drinking 

Water Contaminant Candidate List— 

Preliminary Determinations 

AGENCY: Environmental Protection 

Agency (EPA). 

ACTION: Notice. 

SUMMARY: The Safe Drinking Water Act 

(SDWA), as amended in 1996, requires 

the Environmental Protection Agency 

(EPA) to make regulatory 

determinations on at least five 

unregulated contaminants and decide 

whether to regulate these contaminants 

with a national primary drinking water 

regulation (NPDWR). SDWA requires 

that these determinations be made every 

five years. These unregulated 

contaminants are typically chosen from 

a list known as the Contaminant 

Candidate List (CCL), which SDWA 

requires the Agency to publish every 

five years. EPA published the second 

CCL (CCL 2) in the Federal Register on 

February 24, 2005 (70 FR 9071 (USEPA, 

2005a)). This action presents the 

preliminary regulatory determinations 

for 11 of the 51 contaminants listed on 

CCL 2 and describes the supporting 

rationale for each. The preliminary 

determination is that an NPDWR is not 

appropriate for any of the 11 

contaminants considered for regulatory 

determinations. The Agency seeks 

comment on these 11 preliminary 

determinations. While the Agency has 

not made a preliminary determination 

for perchlorate, this action provides an 

update on the Agency’s evaluation of 

perchlorate. The Agency requests public 

comment on the information and the 

options that the Agency is considering 

in evaluating perchlorate and welcomes 

the submission of relevant, new 

information and/or data that may assist 

the Agency in its regulatory 

determination. 

DATES: Comments must be received on 

or before July 2, 2007. 

ADDRESSES: Submit your comments, 

identified by Docket ID No. EPA–HQ– 

OW–2007–0068, by one of the following 

methods: 

<bullet≤ http://www.regulations.gov: 

Follow the online instructions for 

submitting comments. <bullet≤ Mail: Water Docket, 

Environmental Protection Agency, 

Mailcode: 2822T, 1200 Pennsylvania 

Ave., NW., Washington, DC 20460. 

<bullet≤ Hand Delivery: Water 

Docket, EPA Docket Center (EPA/DC). 

Such deliveries are only accepted 

during the Docket’s normal hours of 

operation, and special arrangements 

should be made for deliveries of boxed 

information. 

Instructions: Direct your comments to 

Docket ID No. EPA–HQ–OW–2007– 

0068. EPA’s policy is that all comments 

received will be included in the public 

docket without change and may be 

made available online at http:// 

www.regulations.gov, including any 

personal information provided, unless 

the comment includes information 

claimed to be Confidential Business 

Information (CBI) or other information 

whose disclosure is restricted by statute. 

Do not submit information that you 

consider to be CBI or otherwise 

protected through http:// 

www.regulations.gov. The http:// 

www.regulations.gov Web site is an 

‘‘anonymous access’’ system, which 

means EPA will not know your identity 

or contact information unless you 

provide it in the body of your comment. 

If you send an e-mail comment directly 

to EPA without going through http:// 

www.regulations.gov your e-mail 

address will be automatically captured 

and included as part of the comment 

that is placed in the public docket and 

made available on the Internet. If you 

submit an electronic comment, EPA 

recommends that you include your 

name and other contact information in 

the body of your comment and with any 

disk or CD–ROM you submit. If EPA 

cannot read your comment due to 

technical difficulties and cannot contact 

you for clarification, EPA may not be 

able to consider your comment. 

Electronic files should avoid the use of 

special characters, any form of 

encryption, and be free of any defects or 

viruses. For additional instructions on 

submitting comments, go to Unit I.B of 

the SUPPLEMENTARY INFORMATION section 

of this document. 

Docket: All documents in the docket 

are listed in the http:// 

www.regulations.gov index. Although 

listed in the index, some information is 

not publicly available, e.g., CBI or other 

information whose disclosure is 

restricted by statute. Certain other 

material, such as copyrighted material, 

will be publicly available only in hard 

copy. Publicly available docket 

materials are available either 

electronically in http:// 

www.regulations.gov or in hard copy at 

the Water Docket, EPA/DC, EPA West, 

Room 3334, 1301 Constitution Ave., 

NW., Washington, DC. The Public 

Reading Room is open from 8:30 a.m. to 

4:30 p.m., Monday through Friday, 

excluding legal holidays. The telephone 

number for the Public Reading Room is 

(202) 566–1744, and the telephone 

number for the EPA Docket Center is 

(202) 566–2426. 

FOR FURTHER INFORMATION CONTACT: 

Wynne Miller, Office of Ground Water 

and Drinking Water, Standards and Risk 

Management Division, at (202) 564– 

4887 or e-mail miller.wynne@epa.gov. 

For general information contact the EPA 

Safe Drinking Water Hotline at (800) 

426–4791 or e-mail: hotlinesdwa@epa.gov. 

SUPPLEMENTARY INFORMATION: 

Abbreviations and Acronyms 

a. i.—active ingredient 

<—less than 

<=—less than or equal to 

≤—greater than 

≤=—greater than or equal to 

[mu]—microgram, one-millionth of a gram 

[mu]g/g—micrograms per gram 

[mu]g/kg—micrograms per kilogram 

[mu]g/L—micrograms per liter 

ATSDR—Agency for Toxic Substances and 

Disease Registry 

AWWARF—American Water Works 

Association Research Foundation 

BMD—bench mark dose 

BMDL—bench mark dose level 

BW—body weight for an adult, assumed to be 

70 kilograms (kg) 

CASRN—Chemical Abstract Services 

Registry Number 

CBI—confidential business information 

CDC—Centers for Disease Control and 

Prevention 

ChE—cholinesterase 

CCL—Contaminant Candidate List 

CCL 1—EPA’s First Contaminant Candidate 

List 

CCL 2—EPA’s Second Contaminant 

Candidate List 

CFR—Code of Federal Regulations 

CMR—Chemical Monitoring Reform 

CWS—community water system 

1,3-DCP—1,3-dichloropropene 

DCPA—dimethyl tetrachloroterephthalate 

(dacthal) 

DDE—1,1-dichloro-2,2-bis(pchlorophenyl)ethylene 

DDT—1,1,1-trichloro-2,2-bis(pchlorophenyl)ethane 

DNT—dinitrotoluene 

DW—dry weight 

DWEL—drinking water equivalent level 

DWI—drinking water intake, assumed to be 

2 L/day 

EPA—United States Environmental 

Protection Agency 

EPCRA—Emergency Planning and 

Community Right-to-Know Act 

EPTC—s-ethyl dipropylthiocarbamate 

ESA—ethane sulfonic acid 

FDA—United States Food and Drug 

Administration 

FQPA—Food Quality Protection Act 

FR—Federal Register 

FW—fresh weight 

g—gram 

g/day—grams per day 


rmajette on DSK29S0YB1PROD with MISCELLANEOUS
Federal Register / Vol. 72, No. 83 / Tuesday, May 1, 2007 / Proposed Rules 24017 

HRL—health reference level 

IOC—inorganic compound 

IRIS—Integrated Risk Information System 

kg—kilogram 

L—liter 

LD50—an estimate of a single dose that is 

expected to cause the death of 50 percent 

of the exposed animals; it is derived 

from experimental data. 

LOAEL—lowest-observed-adverse-effect level 

MAC—mycobacterium avium intercellulare 

MCL—maximum contaminant level 

MCLG—maximum contaminant level goal 

mg—milligram, one-thousandth of a gram 

mg/kg—milligrams per kilogram body weight 

mg/kg/day—milligrams per kilogram body 

weight per day 

mg/L—milligrams per liter 

mg/m3—milligrams per cubic meter 

MRL—minimum or method reporting limit 

(depending on the study or suvey cited) 

MTBE—methyl tertiary butyl ether 

MTP—monomethyl-2,3,5,6- 

tetrachloroterephthalate 

N—number of samples 

NAS—National Academies of Sciences 

NAWQA—National Water Quality 

Assessment (USGS Program) 

NCEH—National Center for Environmental 

Health (CDC) 

NCFAP—National Center for Food and 

Agricultural Policy 

NCI—National Cancer Institute 

NCWS—non community water system 

ND—not detected (or non detect) 

NDWAC—National Drinking Water Advisory 

Council 

NHANES—National Health and Nutrition 

Examination Survey (CDC) 

NIRS—National Inorganic and Radionuclide 

Survey 

NIS—sodium iodide symporter 

NOEL—no-observed-effect-level 

NOAEL—no-observed-adverse-effect level 

NPS—National Pesticide Survey 

NQ—not quantifiable (or non quantifiable) 

NRC—National Research Council 

NPDWR—National Primary Drinking Water 

Regulation 

NTP—National Toxicology Program 

OA—oxanilic acid 

OW—Office of Water 

OPP—Office of Pesticide Programs 

PCR—Polymerase Chain Reaction 

PGWDB—pesticides in ground water data 

base 

PWS—public water system 

RED—Reregistration Eligibility Decision 

RfC—reference concentration 

RfD—reference dose 

RSC—relative source contribution 

SAB—Science Advisory Board 

SDWA—Safe Drinking Water Act 

SOC—synthetic organic compound 

SVOC—semi-volatile organic compound 

T3—triiodothyronine 

T4—thyroxine 

TDS—Total Diet Study (FDA) 

Tg-DNT—technical grade DNT 

TPA—2,3,5,6-tetrachchloroterephthalic acid 

TRI—Toxics Release Inventory 

TSH—thyroid stimulating hormone 

TT—treatment technique 

UCM—Unregulated Contaminant Monitoring 

UCMR 1—First Unregulated Contaminant 

Monitoring Regulation 

UF—uncertainty factor 

US—United States of America 

USDA—United States Department of 

Agriculture 

USGS—United States Geological Survey 

UST—underground storage tanks 

VOC—volatile organic compound 

I. General Information 

A. Does This Action Impose Any 

Requirements on My Public Water 

System? 

B. What Should I Consider as I Prepare My 

Comments for EPA? 

II. Purpose, Background and Summary of 

This Action 

A. What Is the Purpose of This Action? 

B. Background on the CCL and Regulatory 

Determinations 

C. Summary of the Approach Used To 

Identify and Evaluate Candidates for 

Regulatory Determination 2 

D. What Are EPA’s Preliminary 

Determinations and What Happens Next? 

E. Supporting Documentation for EPA’s 

Preliminary Determinations 

III. What Analyses Did EPA Use To Support 

the Preliminary Regulatory 

Determinations? 

A. Evaluation of Adverse Health Effects 

B. Evaluation of Contaminant Occurrence 

and Exposure 

IV. Preliminary Regulatory Determinations 

A. Summary of the Preliminary Regulatory 

Determination 

B. Contaminant Profiles 

1. Boron 

2. and 3. Mono- and Di-Acid Degradates of 

Dimethyl Tetrachloroterephthalate 

(DCPA) 

4. 1,1-Dichloro-2,2-bis(p-chlorophenyl) 

ethylene (DDE) 

5. 1,3-Dichloropropene (1,3-DCP; Telone) 

6. and 7. 2,4- and 2,6-Dinitrotoluenes (2,4- 

and 2,6-DNT) 

8. s-Ethyl dipropylthiocarbamate (EPTC) 

9. Fonofos 

10. Terbacil 

11. 1,1,2,2-Tetrachloroethane 

V. What Is the Status of the Agency’s 

Evaluation of Perchlorate? 

A. Sources of Perchlorate 

B. Health Effects 

C. Occurrence in Water, Food, and 

Humans. 

D. Occurrence Studies on Perchlorate in 

Human Urine, Breast Milk, and Amniotic 

Fluid 

E. Status of the Preliminary Regulatory 

Determination for Perchlorate 

F. What Are the Potential Options for 

Characterizing Perchlorate Exposure and 

Proceeding With the Preliminary 

Regulatory Determination for 

Perchlorate? 

G. Next Steps 

VI. What About the Remaining CCL 2 

Contaminants? 

A. Metolachlor 

B. Methyl tertiary-butyl ether 

C. Microbial Contaminants 

VII. EPA’s Next Steps 

VIII. References 

I. General Information 

A. Does This Action Impose Any 

Requirements on My Public Water 

System? 

None of these preliminary regulatory 

determinations or the final regulatory 

determinations, when published, will 

impose any requirements on anyone. 

Instead, this action notifies interested 

parties of the availability of EPA’s 

preliminary regulatory determinations 

for 11 of the 51 contaminants listed on 

CCL 2 and seeks comment on these 

preliminary determinations. This action 

also provides an update on the Agency’s 

review of perchlorate and methyl 

tertiary butyl ether (MTBE). 

B. What Should I Consider as I Prepare 

My Comments for EPA? 

You may find the following 

suggestions helpful for preparing your 

comments: 

1. Explain your views as clearly as 

possible. 

2. Describe any assumptions that you 

used. 

3. Provide any technical information 

and/or data you used that support your 

views. 

4. If you estimate potential burden or 

costs, explain how you arrived at your 

estimate. 

5. Provide specific examples to 

illustrate your concerns. 

6. Offer alternatives. 

7. Make sure to submit your 

comments by the comment period 

deadline. 

8. To ensure proper receipt by EPA, 

identify the appropriate docket 

identification number in the subject line 

on the first page of your response. It 

would also be helpful if you provided 

the name, date, and Federal Register 

citation related to your comments. 

II. Purpose, Background and Summary 

of This Action 

This section briefly summarizes the 

purpose of this action, the statutory 

requirements, previous activities related 

to the Contaminant Candidate List and 

regulatory determinations, and the 

approach used and outcome of these 

preliminary regulatory determinations. 

A. What Is the Purpose of This Action? 

The Safe Drinking Water Act (SDWA), 

as amended in 1996, requires EPA to 

publish a list of currently unregulated 

contaminants that may pose risks for 

drinking water (referred to as the 

Contaminant Candidate List, or CCL) 

and to make determinations on whether 

to regulate at least five contaminants 

from the CCL with a national primary 

drinking water regulation (NPDWR) 


rmajette on DSK29S0YB1PROD with MISCELLANEOUS
24018 Federal Register / Vol. 72, No. 83 / Tuesday, May 1, 2007 / Proposed Rules 

1 The MCLG is the ‘‘maximum level of a 

contaminant in drinking water at which no known 

or anticipated adverse effect on the health of 

persons would occur, and which allows an 

adequate margin of safety. Maximum contaminant 

level goals are nonenforceable health goals’’ (40 

CFR 141.2). 

2 An NPDWR is a legally enforceable standard 

that applies to public water systems. An NPDWR 

sets a legal limit (called a maximum contaminant 

level or MCL) or specifies a certain treatment 

technique (TT) for public water systems for a 

specific contaminant or group of contaminants. 

3 The statute authorizes a nine month extension 

of this promulgation date. 

(section 1412(b)(1)). The 1996 SDWA 

requires the Agency to publish both the 

CCL and the regulatory determinations 

every five years. The purpose of this 

action is to present (1) EPA’s 

preliminary regulatory determinations 

for 11 candidates selected from the 51 

contaminants listed on the second CCL 

(CCL 2), (2) the process and the 

rationale used to make these 

determinations, and (3) a brief summary 

of the supporting documentation. This 

action also includes a request for 

comment(s) on the Agency’s 

preliminary determinations. 

The 11 regulatory determination 

contaminants candidates discussed in 

this action are boron, the dacthal monoand di-acid degradates, 1,1-dichloro-2,2- 

bis(p-chlorophenyl)ethylene (DDE), 1,3- 

dichloropropene, 2,4-dinitrotoluene, 

2,6-dinitrotoluene, s-ethyl 

propylthiocarbamate (EPTC), fonofos, 

terbacil, and 1,1,2,2-tetrachloroethane. 

B. Background on the CCL and 

Regulatory Determinations 

1. Statutory Requirements for CCL 

and Regulatory Determinations. The 

specific statutory requirements for the 

CCL and regulatory determinations can 

be found in SDWA section 1412(b)(1). 

The 1996 SDWA Amendments require 

EPA to publish the CCL every five years. 

The CCL is a list of contaminants that 

are not subject to any proposed or 

promulgated NPDWRs, are known or 

anticipated to occur in public water 

systems (PWSs), and may require 

regulation under SDWA. The 1996 

SDWA Amendments also direct EPA to 

determine whether to regulate at least 

five contaminants from the CCL every 

five years (within three and one-half 

years after publication of the final list). 

In making regulatory determinations, 

SDWA requires EPA to publish a 

Maximum Contaminant Level Goal 1

(MCLG) and promulgate an NPDWR 2

for a contaminant if the Administrator 

determines that: 

(a) The contaminant may have an 

adverse effect on the health of persons; 

(b) the contaminant is known to occur 

or there is a substantial likelihood that 

the contaminant will occur in public 

water systems with a frequency and at 

levels of public health concern; and 

(c) In the sole judgment of the 

Administrator, regulation of such 

contaminant presents a meaningful 

opportunity for health risk reduction for 

persons served by public water systems. 

If EPA determines that all three of 

these statutory criteria are met and 

makes a final determination that a 

national primary drinking water 

regulation is needed, the Agency has 24 

months to publish a proposed MCLG 

and NPDWR. After the proposal, the 

Agency has 18 months to publish and 

promulgate a final MCLG and NPDWR 

(SDWA section 1412(b)(1)(E)).3

2. The First Contaminant Candidate 

List (CCL 1). Following the 1996 SDWA 

Amendments, EPA sought input from 

the National Drinking Water Advisory 

Council (NDWAC) on the process that 

should be used to identify contaminants 

for inclusion on the CCL. For chemical 

contaminants, the Agency developed 

screening and evaluation criteria based 

on recommendations from NDWAC. For 

microbiological contaminants, NDWAC 

recommended that the Agency seek 

external expertise to identify and select 

potential waterborne pathogens. As a 

result, the Agency convened a workshop 

of microbiologists and public health 

experts who developed criteria for 

screening and evaluation and 

subsequently developed an initial list of 

potential microbiological contaminants. 

The first CCL process benefited from 

considerable input from the NDWAC, 

the scientific community, and the 

public through stakeholder meetings 

and the public comments received on 

the draft CCL published on October 6, 

1997 (62 FR 52193 (USEPA, 1997a)). 

EPA published the final CCL, which 

contained 50 chemical and 10 

microbiological contaminants, on March 

2, 1998 (63 FR 10273 (USEPA, 1998a)). 

A more detailed discussion of how EPA 

developed CCL 1 can be found in the 

1997 and the 1998 Federal Register 

notices (62 FR 52193 (USEPA, 1997a) 

and 63 FR 10273 (USEPA, 1998a)). 

3. The Regulatory Determinations for 

CCL 1. EPA published its preliminary 

regulatory determinations for a subset of 

contaminants listed on CCL 1 on June 3, 

2002 (67 FR 38222 (USEPA, 2002a)). 

The Agency published its final 

regulatory determinations on July 18, 

2003 (68 FR 42898 (USEPA, 2003a)). 

EPA identified 9 contaminants from the 

60 contaminants listed on CCL 1 that 

had sufficient data and information 

available to make regulatory 

determinations. The 9 contaminants 

were Acanthamoeba, aldrin, dieldrin, 

hexachlorobutadiene, manganese, 

metribuzin, naphthalene, sodium, and 

sulfate. The Agency determined that a 

national primary drinking water 

regulation was not necessary for any of 

these 9 contaminants. The Agency 

issued guidance on Acanthamoeba and 

health advisories for magnesium, 

sodium, and sulfate. 

The decision-making process that 

EPA used to make its regulatory 

determinations for CCL 1 was based on 

substantial expert input and 

recommendations from different groups 

including stakeholders, the National 

Research Council (NRC) and NDWAC. 

In June 2002, EPA consulted with the 

Science Advisory Board (SAB) Drinking 

Water Committee and requested its 

review and comment on whether the 

protocol EPA developed, based on the 

NDWAC recommendations, was 

consistently applied and appropriately 

documented. SAB provided verbal 

feedback regarding the use of the NRC 

and NDWAC recommendations in EPA’s 

decision criteria for making its 

regulatory determinations. SAB 

recommended that the Agency provide 

a transparent and clear explanation of 

the process for making regulatory 

determinations. The Agency took SAB’s 

recommendation into consideration and 

further explained the CCL 1 regulatory 

determination evaluation process in the 

July 18, 2003 (68 FR 42898 (USEPA, 

2003a)) notice and in the supporting 

documentation. 

EPA has used the same approach to 

develop the regulatory determinations 

discussed in this action. While this 

action includes a short description of 

the decision process used to make 

regulatory determinations (section II.C), 

a more detailed discussion can be found 

in the 2002 and the 2003 Federal 

Register notices (67 FR 38222 (USEPA, 

2002a) and 68 FR 42898 (USEPA, 

2003a)). 

4. The Second Contaminant 

Candidate List (CCL 2). The Agency 

published its draft CCL 2 Federal 

Register notice on April 2, 2004 (69 FR 

17406 (USEPA, 2004a)) and the final 

CCL 2 Federal Register notice on 

February 24, 2005 (70 FR 9071 (USEPA, 

2005a)). The CCL 2 carried forward the 

51 remaining chemical and microbial 

contaminants that were listed on CCL 1. 

5. The Regulatory Determinations for 

CCL 2. This current action discusses 

EPA’s preliminary determinations for 11 

of the 51 contaminants listed on the 

CCL 2. 


rmajette on DSK29S0YB1PROD with MISCELLANEOUS
Federal Register / Vol. 72, No. 83 / Tuesday, May 1, 2007 / Proposed Rules 24019 

4 Health information used for the regulatory 

determinations process includes but is not limited 

to health assessments available from the Agency’s 

Integrated Risk Information System (IRIS), the 

Agency’s Office of Pesticide Programs (OPP) in a 

Reregistration Eligibility Decision (RED), the 

National Academy of Sciences (NAS), and/or the 

Agency for Toxic Substances and Disease Registry 

(ATSDR). 

C. Summary of the Approach Used To 

Identify and Evaluate Candidates for 

Regulatory Determination 2 

Figure 1 provides a brief overview of 

the process EPA used to identify which 

CCL 2 contaminants are candidates for 

regulatory determinations and the 

SDWA statutory criteria considered in 

making the regulatory determinations. 

BILLING CODE 6560–50–P 

BILLING CODE 6560–50–C 

In identifying which CCL 2 

contaminants are candidates for 

regulatory determinations, the Agency 

considered whether sufficient 

information and/or data were available 

to characterize the potential health 

effects and the known/likely occurrence 

in and exposure from drinking water. 

With regards to sufficient health effects 

information/data, the Agency 

considered whether an Agencyapproved health risk assessment 4 was 

available to identify any potential 

adverse health effect(s) and derive an 

estimated level at which adverse health 

effect(s) are likely to occur. With regards 

to sufficient occurrence information/ 

data, the Agency considered whether 

information/data were available to 


rmajette on DSK29S0YB1PROD with MISCELLANEOUSEP01MY07.050
24020 Federal Register / Vol. 72, No. 83 / Tuesday, May 1, 2007 / Proposed Rules 

evaluate and give a generally 

representative idea of known and/or 

likely occurrence in public water 

systems. If sufficient information/data 

were available to characterize adverse 

human health effects and known/likely 

occurrence in public water systems, the 

Agency identified the contaminant as a 

potential candidate for regulatory 

determinations. In addition to 

information/data for health and 

occurrence, EPA also considered the 

availability and adequacy of analytical 

methods (for monitoring) and treatment. 

If EPA chose a contaminant as a 

candidate for regulatory determination, 

the Agency used an approach similar to 

the first regulatory determination 

process to answer the three statutory 

criteria (listed in section II.B.1). 

For the current regulatory 

determination process, the Agency 

considered the following in evaluating 

each of the three statutory criteria. 

(1) First statutory criterion—Is the 

contaminant likely to cause an adverse 

effect on the health of persons? The 

Agency evaluated the best available, 

peer-reviewed assessments and studies 

to characterize the human health effects 

that may result from exposure to the 

contaminant when found in drinking 

water. Based on this characterization, 

the Agency estimated a health reference 

level (HRL) for each contaminant. 

Section III.A provides more detailed 

information about the approach used to 

evaluate and analyze the health 

information. 

(2) Second statutory criterion—Is the 

contaminant known or likely to occur in 

public water systems at a frequency and 

level of concern? To evaluate known 

occurrence in PWSs, the Agency 

compiled, screened, and analyzed data 

from several occurrence data sets to 

develop representative occurrence 

estimates for public drinking water 

systems. EPA used the HRL estimates 

for each contaminant as a benchmark 

against which to conduct an initial 

evaluation or screening of the 

occurrence data. For each contaminant, 

EPA estimated the number of PWSs 

(and the population served by these 

PWSs) with detections greater than onehalf the HRL (≤ 1/2 HRL) and greater 

than the HRL (≤ HRL). To evaluate the 

likelihood of a contaminant to occur in 

drinking water, the Agency considered 

information on the use and release of a 

contaminant into the environment and 

supplemental information on 

occurrence in water (e.g., ambient water 

quality data, State ambient or finished 

water data, and/or special studies 

performed by other agencies, 

organizations and/or entities). Section 

III.B provides more details on the 

approach used to analyze the 

occurrence information/data. 

(3) Third statutory criterion—In the 

sole judgment of the Administrator, 

does regulation of the contaminant 

present a meaningful opportunity for 

health risk reduction for persons served 

by public water systems? EPA evaluated 

the potential health effects and the 

results of the occurrence and exposure 

estimates (i.e., the population exposed 

and the sources of exposure) at the 

health level of concern to determine if 

regulation presents a meaningful 

opportunity for health risk reduction. 

EPA has made a preliminary 

determination regarding the meaningful 

opportunity for health risk reduction for 

11 contaminants based upon the 

population exposed to these 

contaminants at levels of concern. 

If the answers to all three statutory 

criteria are affirmative for a particular 

contaminant, then the Agency makes a 

determination that a national drinking 

water regulation is necessary and 

proceeds to develop an MCLG and a 

national primary drinking water 

regulation for that contaminant. It 

should be noted that this regulatory 

determination process is independent of 

the more detailed analyses needed to 

develop a national primary drinking 

water regulation. Thus, a decision to 

regulate is the beginning of the Agency 

regulatory development process, not the 

end. 

If the answer to any of the three 

statutory criteria is negative, then the 

Agency makes a determination that a 

national drinking water regulation is not 

necessary for that contaminant. 

D. What Are EPA’s Preliminary 

Determinations and What Happens 

Next? 

EPA has made preliminary 

determinations that no regulatory 

actions are appropriate for the 11 

contaminants evaluated for this second 

round of regulatory determinations. EPA 

will make final determinations on these 

11 contaminants after a 60-day comment 

period. EPA is making preliminary 

regulatory determinations only on those 

CCL 2 contaminants that have sufficient 

information to support such a 

determination at this time. The Agency 

continues to conduct research and/or to 

collect information on the remaining 

CCL 2 contaminants to fill identified 

data gaps. The Agency is not precluded 

from taking action when information 

becomes available and will not 

necessarily wait until the end of the 

next regulatory determination cycle 

before making other regulatory 

determinations. 

E. Supporting Documentation for EPA’s 

Preliminary Determinations 

For this action, EPA prepared several 

support documents that are available for 

review and comment in the EPA Water 

Docket and at http:// 

www.regulations.gov. These support 

documents include: 

<bullet≤ A comprehensive regulatory 

support document entitled, ‘‘Regulatory 

Determinations Support Document for 

Selected Contaminants from the Second 

Drinking Water Contaminant Candidate 

List’’ (CCL 2) (USEPA, 2006a). This 

support document summarizes the 

information and data on the physical 

and chemical properties, uses and 

environmental release, environmental 

fate, potential health effects, occurrence 

and exposure estimates, the preliminary 

determination for each contaminant 

candidate, and the Agency’s rationale 

for its determination. The technical 

health and occurrence support 

documents listed next served as the 

basis for the health information and the 

drinking water occurrence estimates 

summarized in this comprehensive 

regulatory support document. 

<bullet≤ Technical health support 

documents. These documents address 

exposure from drinking water and other 

media, toxicokinetics, hazard 

identification, and dose-response 

assessment, and provide an overall 

characterization of the risk from 

drinking water for the contaminants 

considered for regulatory determination. 

These documents are listed in the 

reference section as ‘‘USEPA, 2006j’’ 

through ‘‘USEPA, 2006r.’’ 

<bullet≤ Technical occurrence 

support documents (USEPA, 2006b and 

USEPA, 2006c). These documents 

include more detailed information about 

the sources of the data, how EPA 

assessed the data quality, completeness, 

and representativeness, and how the 

data were used to generate estimates of 

drinking water contaminant occurrence 

in support of these regulatory 

determinations. Section III.B.3 provides 

more information about the title and 

content of these technical support 

documents. 

III. What Analyses Did EPA Use To 

Support the Preliminary Regulatory 

Determinations? 

Sections III.A and B of this action 

outline the health effects and 

occurrence/exposure evaluation process 

EPA used to support these preliminary 

determinations. 

A. Evaluation of Adverse Health Effects 

Section 1412(b)(1)(A)(i) of SDWA 

requires EPA to determine whether each 


rmajette on DSK29S0YB1PROD with MISCELLANEOUS
Federal Register / Vol. 72, No. 83 / Tuesday, May 1, 2007 / Proposed Rules 24021 

5 IRIS is an electronic EPA database (http:// 

www.epa.gov/iris/index.html) containing peerreviewed information on human health effects that 

may result from exposure to various chemicals in 

the environment. These chemical files contain 

descriptive and quantitative information on hazard 

identification and dose response, RfDs for chronic 

noncarcinogenic health effects, as well as slope 

factors and unit risks for carcinogenic effects. 

6 The OPP is required under the Federal 

Insecticide Fungicide and Rodenticide Act (FIFRA) 

to review all pesticides registered prior to 1984 and 

determine whether to reregister them for continued 

use. The results of the reregistration analysis are 

included in the REDs. Copies of the REDs are 

located at the following Web site: http:// 

cfpub.epa.gov/oppref/rereg/status.cfm?show=rereg. 

candidate contaminant may have an 

adverse effect on public health. This 

section describes the overall process the 

Agency used to evaluate health effects 

information, the approach used to 

estimate a contaminant HRL (a 

benchmark against which to conduct the 

initial evaluation of the occurrence 

data), and the approach used to identify 

and evaluate information on hazard and 

dose-response for the contaminants 

under consideration. More specific 

information about the potential for 

adverse health effects for each 

contaminant is presented in section IV.B 

of this action. 

There are two different approaches to 

the derivation of an HRL. One approach 

is used for chemicals that cause cancer 

and exhibit a linear response to dose 

and the other applies to noncarcinogens 

and carcinogens evaluated using a nonlinear approach. 

1. Use of Carcinogenicity Data for the 

Derivation of a Health Reference Level. 

For those contaminants considered to be 

likely or probable human carcinogens, 

EPA evaluated data on the mode of 

action of the chemical to determine the 

method of low dose extrapolation. 

When this analysis indicates that a 

linear low dose extrapolation is 

appropriate or when data on the mode 

of action are lacking, EPA uses a low 

dose linear extrapolation to calculate 

risk-specific doses. The risk-specific 

doses are the estimated oral exposures 

associated with lifetime excess risk 

levels that range from one cancer in ten 

thousand (10-4) to one cancer in a 

million (10-6). The risk-specific doses 

(expressed as mg/kg of body weight per 

day) are combined with adult body 

weight and drinking water consumption 

data to estimate drinking water 

concentrations corresponding to this 

risk range. EPA generally used the onein-a-million (10-6) cancer risk in the 

initial screening of the occurrence data 

for carcinogens evaluated using linear 

low dose extrapolation. Five of the 

eleven contaminants discussed in this 

action had data available to classify 

them as likely or probable human 

carcinogens. These five are also the only 

contaminants for which low dose linear 

extrapolations were performed. These 

five are p,pdichlorodiphenyldichloroethylene 

(DDE), 1,3-dichloropropene (1,3-DCP or 

Telone), 2,4-dinitrotoluene, 2,6- 

dinitrotoluene, and 1,1,2,2- 

tetrachloroethane. The remaining 6 

contaminants have not been identified 

as known, likely or probable 

carcinogens. 

2. Use of Non-carcinogenic Health 

Effects Data for Derivation of an HRL. 

For those chemicals not considered to 

be carcinogenic to humans, EPA 

generally calculates a reference dose 

(RfD). A RfD is an estimate of a daily 

oral exposure to the human population 

(including sensitive subgroups) that is 

likely to be without an appreciable risk 

of deleterious effects during a lifetime. 

It can be derived from either a ‘‘noobserved-adverse-effect level’’ (NOAEL), 

a ‘‘lowest-observed-adverse-effect level’’ 

(LOAEL), or a benchmark dose, with 

uncertainty factors applied to reflect 

limitations of the data used. 

The Agency uses uncertainty factors 

(UFs) to address uncertainty resulting 

from incompleteness of the toxicological 

database. The individual UFs (usually 

applied as integers of 1, 3, or 10) are 

multiplied together and used to derive 

the RfD from experimental data. 

Individual UFs are intended to account 

for: 

(1) The variation in sensitivity among 

the members of the human population 

(i.e., intraspecies variability); 

(2) the uncertainty in extrapolating 

animal data to humans (i.e., interspecies 

variability); 

(3) the uncertainty in extrapolating 

from data obtained in a study with lessthan-lifetime exposure to lifetime 

exposure (i.e., extrapolating from 

subchronic to chronic exposure); 

(4) the uncertainty in extrapolating 

from a LOAEL rather than from a 

NOAEL; and/or 

(5) the uncertainty associated with an 

incomplete database. 

For boron, the dacthal (DCPA) mono 

and di acid degradates, s-ethyl 

dipropylthiocarbamate (EPTC), fonofos 

and terbacil, EPA derived the HRLs 

using the RfD approach as follows: 

HRL = [(RfD x BW)/DWI] x RSC 

Where: 

RfD = Reference Dose 

BW = Body Weight for an adult, assumed to 

be 70 kilograms (kg) 

DWI = Drinking Water Intake, assumed to be 

2 L/day (90th percentile) 

RSC = Relative Source Contribution, or the 

level of exposure believed to result from 

drinking water when compared to other 

sources (e.g., food, ambient air). A 20 

percent RSC is being used to estimate the 

HRL and screen the occurrence data 

because it is the lowest and most 

conservative RSC used in the derivation 

of an MCLG for drinking water. For each 

of the 6 aforementioned noncarcinogenic compounds for which the 

Agency has made a preliminary 

regulatory determination in this action, 

EPA used the RfD in conjunction with a 

20 percent RSC to derive a conservative 

HRL estimate and perform an initial 

screening of the drinking water 

occurrence data. Since the initial 

screening of the occurrence data at this 

conservative HRL value resulted in a 

preliminary negative determination for 

each of these 6 compounds, the Agency 

determined that it was not necessary to 

further evaluate the RSC in making the 

regulatory determination. 

As discussed in section IV.B.2 and 3, 

the HRL for the two dacthal degradates 

is based on the HRL value derived for 

the DCPA parent following the guidance 

provided by EPA’s Office of Pesticide 

Programs. 

3. Sources of Data/Information for 

Health Effects. EPA used the best 

available peer-reviewed data and 

analyses in evaluating adverse health 

effects. Peer-reviewed health-risk 

assessments were available for all 

chemicals considered for regulatory 

determinations from the Agency’s 

Integrated Risk Information System 

(IRIS) Program5 and/or the Office of 

Pesticide Programs (OPP) Reregistration 

Eligibility Decisions (RED).6 Table 1 

summarizes the sources of the health 

assessment data for each chemical 

under regulatory determination 

consideration. The Agency performed a 

literature search for studies published 

after the IRIS or OPP health-risk 

assessment was completed to determine 

if new information suggested a different 

outcome. The Agency collected and 

evaluated any peer-reviewed 

publications identified through the 

literature search for their impact on the 

RfD and/or cancer assessment. In cases 

where the recent data indicated that a 

change to the existing RfD or cancer 

assessment was needed, the updated 

OW assessment, as described in the 

health effects support document, was 

independently peer-reviewed. All 

quantitative cancer assessments 

conducted under the Guidelines for 

Carcinogen Risk Assessment (51 FR 

33992 (USEPA, 1986)) were updated 

using the Guidelines for Carcinogen 

Risk Assessment (USEPA, 1999a) as 

directed in the November 2001 (66 FR 

59593 (USEPA, 2001a)) Federal Register 

notice. 

In March 2005, EPA updated and 

finalized the Cancer Guidelines and a 

Supplementary Children’s Guidance, 


rmajette on DSK29S0YB1PROD with MISCELLANEOUS
24022 Federal Register / Vol. 72, No. 83 / Tuesday, May 1, 2007 / Proposed Rules 

which include new considerations for 

mode of action and added guidelines 

related to potential risks due to early 

childhood exposure (USEPA, 2005b; 

USEPA, 2005c). EPA updated the earlier 

assessments (based on the 1986 

Guidelines) for DDE, the dinitrotoluenes 

(2,4 and 2,6 as a mixture), and 1,1,2,2- 

tetrachloroethane following the 1999 

Guidelines. None of these chemicals 

have been determined to have a 

mutagenic mode of action, which would 

require an extra factor of safety for 

children’s health protection. Therefore, 

conducting the cancer evaluation using 

the 2005 Cancer Guidelines would not 

result in any change from the 

assessment updated following the 1999 

Guidelines. 

The cancer assessment for 1,3- 

dichloropropene was done by OPP and 

IRIS (USEPA, 1998b and 2000a) under 

the Proposed Guidelines for Carcinogen 

Risk Assessment (61 FR 17960 (USEPA, 

1996a)). The Administrator (USEPA, 

2005d) has directed that current 

completed assessments can be 

considered to be scientifically sound 

based on the guidance used when the 

assessment was completed until a new 

assessment is performed by one of the 

responsible program offices. 

TABLE 1.—SOURCES AND DATES OF EPA HEALTH RISK ASSESSMENTS

Chemical IRIS Date OPP RED Date 

Boron ............................................................................................................................... X 2004 .................... ....................

Dacthal and its mono- and di-acid degradates ............................................................... X 1994 X 1998 

1,3-Dichloropropene ........................................................................................................ X 2000 X 1998 

DDE ................................................................................................................................. X 1988 .................... ....................

2,4-Dinitrotoluene ............................................................................................................. X 1990/1992 .................... ....................

2,6-Dinitrotoluene ............................................................................................................. * X 1990 .................... ....................

EPTC ............................................................................................................................... X 1990 X 1999 

Fonofos ............................................................................................................................ X 1991 ** X 1996 

Terbacil ............................................................................................................................ X 1989 X 1998 

1,1,2,2-Tetrachloroethane ................................................................................................ X 1986 .................... ....................

* Applies to a mixture of 98 percent 2,4-dinitrotoluene and 2 percent 2,6-dinitrotoluene. 

** Health Risk Assessment; RED not completed due to pesticide cancellation. 

As noted in section II.E, EPA has 

prepared several technical health effects 

support documents for the contaminants 

considered for this round of regulatory 

determinations. These documents 

address the exposure from drinking 

water and other media, toxicokinetics, 

hazard identification, and dose-response 

assessment, and provide an overall 

characterization of risk from drinking 

water. 

B. Evaluation of Contaminant 

Occurrence and Exposure 

EPA used data from several sources to 

evaluate occurrence and exposure for 

the 11 contaminants considered in these 

regulatory determinations. The major or 

primary sources of the drinking water 

occurrence data used to support these 

determinations include the following 

sources: 

<bullet≤ The first Unregulated 

Contaminant Monitoring Regulation 

(UCMR 1), 

<bullet≤ The Unregulated 

Contaminant Monitoring (UCM) 

program, and 

<bullet≤ The National Inorganic and 

Radionuclide Survey (NIRS). 

In addition to these primary sources 

of occurrence data, the Agency also 

evaluated supplemental sources of 

occurrence information. Section III.B.1 

of this action provides a brief summary 

of the primary sources of drinking water 

occurrence data and section III.B.2 

provides brief summary descriptions of 

the supplemental sources of occurrence 

information and/or data. A summary of 

the occurrence data and the results or 

findings for each of the 11 contaminants 

considered for regulatory determination 

is presented in Section IV.B, the 

contaminant profiles section. 

1. Primary Data Sources. As 

previously mentioned, the primary 

sources of the drinking water 

occurrence data used to support this 

action are the UCMR 1, the UCM 

program, and NIRS. The following 

sections provide a brief summary of the 

data sources and the approach used to 

estimate a given contaminant’s 

occurrence. Table 2 lists the primary 

data sources the Agency used for each 

of the 11 contaminants considered for 

regulatory determinations. 

TABLE 2.—PRIMARY SOURCES OF DRINKING WATER OCCURRENCE DATA USED IN THE REGULATORY DETERMINATION

PROCESS

Number Contaminant 

Primary data sources 

UCMR 1 UCM 

List 1 NIRS 

assessment 

monitoring 

List 2 

screening 

survey 

Round 1 

cross section 

Round 2 

cross section 

1 ........................ Boron .................................................................... 1 X 

2 ........................ Dacthal mono- and 

3 ........................ di-acid degradates ................................................ X 

4 ........................ DDE ...................................................................... X 

5 ........................ 1,3-Dichloropropene ............................................. 2 X X X 

6 ........................ 2,4-Dinitrotoluene ................................................. X 

7 ........................ 2,6-Dinitrotoluene ................................................. X 

8 ........................ EPTC .................................................................... X 

9 ........................ Fonofos ................................................................ X 

10 ...................... Terbacil ................................................................. X 


rmajette on DSK29S0YB1PROD with MISCELLANEOUS
Federal Register / Vol. 72, No. 83 / Tuesday, May 1, 2007 / Proposed Rules 24023 

7 Systems serving more than 10,000 people. 

8 Systems serving 10,000 people or fewer. 

9 Large and small systems that purchase 100% of 

their water supply were not required to participate 

in the UCMR 1 Assessment Monitoring or the 

UCMR 1 Screening Survey. 

10 EPA’s support documents (USEPA, 2006a and 

2006b) provide summary statistics for the median 

and 99th percentile concentrations of all analytical 

detections and detailed occurrence results based on 

UCMR data according to source water type (surface 

versus ground water), system size, and State. 

TABLE 2.—PRIMARY SOURCES OF DRINKING WATER OCCURRENCE DATA USED IN THE REGULATORY DETERMINATION

PROCESS—Continued 

Number Contaminant 

Primary data sources 

UCMR 1 UCM 

List 1 NIRS 

assessment 

monitoring 

List 2 

screening 

survey 

Round 1 

cross section 

Round 2 

cross section 

11 ...................... 1,1,2,2-Tetrachloroethane .................................... X X 

1 For boron, EPA also considered the results of a study funded by AWWARF (Frey et al., 2004). 2 1,3-Dichloropropene was sampled as a UCM Round 1 and 2 analyte but due to sample degradation concerns the contaminant was re-analyzed using the samples provided by the small systems that participated in the UCMR 1 List 1 Assessment Monitoring. 

a. The Unregulated Contaminant 

Monitoring Regulation. In 1999, EPA 

developed the UCMR program in 

coordination with the CCL and the 

National Drinking Water Contaminant 

Occurrence Database (NCOD) to provide 

national occurrence information on 

unregulated contaminants (September 

17, 1999, 64 FR 50556 (USEPA, 1999b); 

March 2, 2000, 65 FR 11372 (USEPA, 

2000b); and January 11, 2001, 66 FR 

2273 (USEPA, 2001b)). EPA used data 

from the UCMR 1 program to evaluate 

occurrence for 9 of the 11 contaminants 

considered for these regulatory 

determinations. These 9 contaminants 

include the dacthal mono- and di-acid 

degradates, DDE, 1,3-dichloropropene, 

2,4-dinitrotoluene, 2,6-dinitrotoluene, 

EPTC, fonofos, and terbacil. 

EPA designed the UCMR 1 data 

collection with three parts (or tiers) 

primarily based on the availability of 

analytical methods. Occurrence data for 

8 of the 9 contaminants listed in the 

preceding paragraph are from the first 

tier of UCMR (also known as UCMR 1 

List 1 Assessment Monitoring). 

Occurrence data for fonofos are from the 

second tier of UCMR 1 (also known as 

the UCMR 1 List 2 Screening Survey). 

EPA has not collected data as part of the 

third tier due to the lack of adequate 

analytical methods. 

The UCMR 1 List 1 Assessment 

Monitoring was performed for a 

specified number of chemical 

contaminants for which analytical 

methods have been developed. EPA 

required all large7 PWSs, plus a 

statistically representative national 

sample of 800 small 8 PWSs to conduct 

Assessment Monitoring.9

Approximately one-third of the 

participating small systems were 

scheduled to monitor for these 

contaminants during each calendar year 

from 2001 through 2003. Large systems 

could conduct one year of monitoring 

anytime during the 2001–2003 UCMR 1 

period. EPA specified a quarterly 

monitoring schedule for surface water 

systems and a twice-a-year, six-month 

interval monitoring schedule for ground 

water systems. The objective of the 

UCMR 1 sampling approach for small 

systems was to collect contaminant 

occurrence data from a statistically 

selected, nationally representative 

sample of small systems. The small 

system sample was stratified and 

population-weighted, and included 

some other sampling adjustments such 

as allocating a selection of at least 2 

systems from each State. With 

contaminant monitoring data from all 

large PWSs and a statistical, nationally 

representative sample of small PWSs, 

the UCMR 1 List 1 Assessment 

Monitoring program provides a 

contaminant occurrence data set 

suitable for national drinking water 

estimates. 

In total, 370,312 sample results have 

been collected under the UCMR 1 List 

1 Assessment Monitoring program at 

approximately 3,083 large systems and 

797 small systems. Approximately 

33,600 samples were collected for each 

contaminant. The UCMR 1 List 1 

Monitoring program included systems 

from all 50 States, the District of 

Columbia, 4 U.S. Territories, and Tribal 

lands in 5 EPA Regions. An additional 

3,719 samples were collected for 1,3- 

DCP at all small systems that conducted 

UCMR 1 List 1 Assessment Monitoring. 

In addition to the UCMR 1 List 1 

Assessment Monitoring, EPA required 

monitoring for selected contaminants 

(including fonofos) for which analytical 

methods were developed but not widely 

used. Known as the UCMR 1 List 2 

Screening Survey, EPA randomly 

selected 300 public water systems (120 

large and 180 small systems) from the 

pool of systems required to conduct 

UCMR 1 List 1 Assessment Monitoring. 

In total, 29,765 sample results have been 

collected under the UCMR 1 List 2 

Screening Survey from the participating 

large and small systems. Approximately 

2,300 samples were collected for each 

contaminant. The UCMR 1 List 2 

Screening Survey included systems 

from 48 States, 2 U.S. Territories, and 

Tribal lands in 1 EPA Region. EPA used 

the occurrence data from this survey to 

evaluate fonofos. 

EPA analyzed the UCMR 1 List 1 

Assessment Monitoring and List 2 

Screening Survey data to generate the 

following initial occurrence and 

exposure summary statistics: 

<bullet≤ The total number of systems 

and the total population served by these 

systems, 

<bullet≤ The number and percentage 

of systems with at least 1 observed 

detection that has a concentration 

greater than 1⁄2 the HRL and greater than 

the HRL (or in some cases greater than 

or equal to the minimum reporting limit 

or MRL), and 

<bullet≤ The number of people and 

percentage of the population served by 

systems with at least one observed 

detection greater than 1⁄2 the HRL and 

greater than the HRL (or in some cases 

greater than or equal to the MRL).10

The initial UCMR 1 summary 

occurrence statistics for dacthal monoand di-acid degradates, DDE, 1,3- 

dichloropropene, 2,4-dinitrotoluene, 

2,6-dinitrotoluene, EPTC, fonofos, and 

terbacil are presented in section IV.B of 

this action. 

b. The Unregulated Contaminant 

Monitoring Program Rounds 1 and 2. In 

1987, EPA initiated the UCM program to 

fulfill a 1986 SDWA Amendment that 

required monitoring of specified 

unregulated contaminants to gather 

information on their occurrence in 

drinking water for future regulatory 

decision-making purposes. EPA used 

data from the UCM program to evaluate 


rmajette on DSK29S0YB1PROD with MISCELLANEOUS
24024 Federal Register / Vol. 72, No. 83 / Tuesday, May 1, 2007 / Proposed Rules 

11 The potential bias in the raw UCM data are due 

to lack of representativeness (since not all States 

provided UCM data) and incompleteness (since 

some States that provided data had incomplete data 

sets). 

12 EPA’s support documents (USEPA, 2006a and 

2006c) provide summary statistics for the median 

and 99th percentile concentrations of all analytical 

detections and detailed occurrence results based on 

the UCM Round 1 and 2 Nationals Cross-Sectons 

according to source water type (surface versus 

ground water), system size, and State. 13 NIRS was designed to provide results that are 

statistically representative of natioal occurrence at 

CWSs using ground water sources and is stratified 

based on system size (population served by the 

system). Most of the NIRS data are from smaller 

systems (92 percent from systems serving 3,300 

persons or fewer). 

14 EPA’s support documents (USEPA, 2006a and 

2006c) provide the number and percentage of 

systems with detections, the 99th percentile 

concentration of all samples, the 99th percentile 

concentration of samples with detections, and the 

median concentration of samples with detections. 

occurrence for 2 of the 11 contaminants 

considered for these regulatory 

determinations. These two 

contaminants are 1,3-dichloropropene 

and 1,1,2,2-tetrachloroethane. 

EPA implemented the UCM program 

in two phases or rounds. The first round 

of UCM monitoring generally extended 

from 1988 to 1992 and is referred to as 

UCM Round 1 monitoring. The second 

round of UCM monitoring generally 

extended from 1993 to 1997 and is 

referred to as UCM Round 2 monitoring. UCM Round 1 monitored for 34 

volatile organic compounds (VOCs), 

including 1,3-dichloropropene and 

1,1,2,2-tetrachloroethane (52 FR 25720 

(USEPA, 1987)). UCM Round 2 

monitored for 13 synthetic organic 

compounds (SOCs), sulfate and the 

same 34 VOCs from UCM Round 1 

monitoring (57 FR 31776 (USEPA, 

1992a)). 

The UCM Round 1 database contains 

contaminant occurrence data from 38 

States, Washington, DC, and the U.S. 

Virgin Islands. The UCM Round 2 

database contains data from 34 States 

and several Tribes. Due to incomplete 

State data sets, national occurrence 

estimates based on raw (unedited) UCM 

Round 1 or Round 2 data could be 

skewed to low-occurrence or highoccurrence settings (e.g., some States 

only reported detections). To address 

potential biases in the data,11 EPA 

developed national cross-sections from 

the UCM Round 1 and Round 2 State 

data using an approach similar to that 

used for EPA’s 1999 Chemical 

Monitoring Reform (CMR), the first Six 

Year Review, and the first CCL 

Regulatory Determinations. This 

national cross-section approach was 

developed to support occurrence 

analyses and was supported by 

scientific peer reviewers and 

stakeholders. This approach identified 

24 of the original 38 States from the 

UCM Round 1 database and 20 of the 

original 34 States from the UCM Round 

2 data base for the national crosssection. 

Because UCM Round 1 and Round 2 

data represent different time periods 

and include occurrence data from 

different States, EPA developed separate 

national cross-sections for each data set. 

The UCM Round 1 national crosssection consists of data from 24 States, 

with approximately 3.3 million total 

analytical data points from 

approximately 22,000 unique PWSs. 

The UCM Round 2 national crosssection consists of data from 20 States, 

with approximately 3.7 million 

analytical data points from slightly more 

than 27,000 unique PWSs. The UCM 

Round 1 and 2 national cross-sections 

represent significantly large samples of 

national occurrence data. Within each 

cross-section, the actual number of 

systems and analytical records for each 

contaminant varies. The support 

document, ‘‘The Analysis of Occurrence 

Data from the Unregulated Contaminant 

Monitoring (UCM) Program and 

National Inorganics and Radionuclides 

Survey (NIRS) in Support of Regulatory 

Determinations for the Second Drinking 

Water Contaminant Candidate List’’ 

(USEPA, 2006c), provides a description 

of how the national cross-sections for 

the Round 1 and Round 2 data sets were 

developed. EPA constructed the national crosssections in a way that provides a 

balance and range of States with varying 

pollution potential indicators, a wide 

range of the geologic and hydrologic 

conditions, and a very large sample of 

monitoring data points. While EPA 

recognizes that some limitations exist, 

the Agency believes that the national 

cross-sections do provide a reasonable 

estimate of the overall distribution and 

the central tendency of contaminant 

occurrence across the United States. 

EPA analyzed the UCM Round 1 and 

2 National Cross-Section data to 

generate the following initial occurrence 

and exposure summary statistics: <bullet≤ The total number of systems 

and the total population served by these 

systems, <bullet≤ The number and percentage 

of systems with at least 1 observed 

detection that has a concentration 

greater than 1⁄2 the HRL and greater than 

the HRL (or in some cases greater than 

or equal to the MRL), and <bullet≤ The number of people and 

percentage of the population served by 

systems with at least 1 observed 

detection that has a concentration 

greater than 1⁄2 the HRL and greater than 

the HRL (or in some cases greater than 

or equal to the MRL).12

The initial UCM summary occurrence 

statistics for 1,3-dichloropropene and 

1,1,2,2-tetrachloroethane are presented 

in section IV.B of this action. c. National Inorganic and 

Radionuclide Survey. In the mid-1980’s, 

EPA conducted the NIRS to provide a 

statistically representative sample 13 of 

the national occurrence of inorganic 

contaminants in community water 

systems (CWSs) served by ground water. 

EPA used data from NIRS, as well as a 

supplemental survey, to evaluate 

occurrence for boron. 

The NIRS database includes 36 

radionuclides and inorganic compounds 

(IOCs), including boron. The NIRS 

provides contaminant occurrence data 

from 989 ground water CWSs covering 

49 States (all except Hawaii) and does 

not include surface water systems. The 

survey focused on ground water 

systems, in part because IOCs tend to 

occur more frequently and at higher 

concentrations in ground water than in 

surface water. Each of the 989 randomly 

selected CWSs was sampled at a single 

time between 1984 and 1986. 

EPA analyzed the NIRS data to 

generate the following occurrence and 

exposure summary statistics for boron: 

<bullet≤ The total number of systems 

and the total population served by these 

systems, 

<bullet≤ The number and the 

percentage of systems with at least 1 

detection that has a concentration 

greater than 1⁄2 the HRL and greater than 

the HRL, 

<bullet≤ The number of people and 

percentage of the population served by 

systems with at least 1 observed 

detection that has a concentration 

greater than 1⁄2 the HRL and greater than 

the HRL.14

Similar to the treatment of the UCM 

cross-section data, the actual values for 

the NIRS analyses of boron are reported 

in section IV.B. Because the NIRS data 

were collected in a randomly designed 

sample survey, these summary statistics 

are representative of national 

occurrence in ground water CWSs. 

One limitation of the NIRS is a lack 

of occurrence data for surface water 

systems. To provide perspective on the 

occurrence of boron in surface water 

systems relative to ground water 

systems, EPA reviewed and took into 

consideration a recent boron occurrence 

survey funded by American Water 

Works Association Research Foundation 

(AWWARF) (Frey et al., 2004). A short 

description of the AWWARF study is 

provided in the supplemental section 


rmajette on DSK29S0YB1PROD with MISCELLANEOUS
Federal Register / Vol. 72, No. 83 / Tuesday, May 1, 2007 / Proposed Rules 24025 

(section III.B.2) and the results of the 

AWWARF survey are presented in 

section IV.B of this action. 

d. Presentation of Occurrence Data 

and Analytical Approach. As noted 

previously, the occurrence values and 

summary statistics presented in this 

action are the actual data from the 

UCMR 1, UCM, and NIRS data sets. 

These occurrence values represent 

direct counts of the number and percent 

of systems, and population served by 

systems, with at least 1 analytical 

detection above some specified 

concentration threshold. EPA 

considered this to be the most 

straightforward and accurate way to 

present these data for the regulatory 

determination process. 

While both UCMR 1 and UCM data 

could support more involved statistical 

modeling to characterize occurrence 

based on mean (rather than peak) 

concentrations, EPA chose not to 

perform this step for the regulatory 

determinations proposed in this action. 

EPA believes that presenting the actual 

results of the occurrence monitoring is 

straight-forward and the use of an 

analysis based on peak concentrations 

provides conservative estimates of 

occurrence and potential exposure from 

drinking water. Given that the 

preliminary determinations for the 11 

contaminants discussed in this action 

are negative, it is not necessary to go 

beyond the conservative (peak 

concentration) approach used for this 

analysis. 

2. Supplemental Data. The Agency 

evaluated several sources of 

supplemental occurrence information to 

augment the primary drinking water 

occurrence data, to evaluate the 

likelihood of contaminant occurrence, 

and/or to more fully characterize a 

contaminant’s presence in the 

environment. Sections II.B.2.a through 

II.B.2.f provide brief descriptions of the 

main supplemental information/data 

sources cited in this action. 

Summarized occurrence findings from 

these supplemental sources are 

presented in Section IV.B, the 

contaminant profiles section. While the 

following descriptions cover the more 

commonly referenced supplemental 

sources of information/data, they do not 

include every study and survey cited in 

the contaminant discussions. A more 

detailed discussion of the supplemental 

sources of information/data that EPA 

evaluated for each contaminant can be 

found in the comprehensive regulatory 

determination support document 

(USEPA, 2006a). 

a. USGS NAWQA Information/Data. 

The United States Geological Survey 

(USGS) collects long-term and 

nationally consistent data describing 

water quality in ground water and 

surface water. In 1991, USGS 

implemented the National WaterQuality Assessment (NAWQA) Program 

for 10-year cyclical data collection and 

data analyses. During the first cycle 

(1991–2001), the NAWQA program 

monitored 51 major watersheds and 

aquifers (study units), which supply 

more than 60% of the nation’s drinking 

water and water used for agriculture and 

industry in the U.S. (Hamilton et al., 

2004). NAWQA has collected data from 

over 6,400 surface water and 7,000 

ground water sampling points. USGS 

National Synthesis teams prepare 

comprehensive analyses of data on 

topics of particular concern. EPA 

evaluated information/data from the 

following USGS National Synthesis 

reports/projects: 

(1) The NAWQA Pesticide National 

Synthesis Project. In 2003, USGS posted 

the preliminary results from the first 

cycle of monitoring for pesticides in 

streams and ground water. USGS 

considers these results to be provisional. 

The results and the data can be accessed 

at http://ca.water.usgs.gov/pnsp/. Data 

are presented separately for surface 

water and ground water, as well as bed 

sediments and biota. In each case, 

results are subdivided by land use 

category. Land use categories include 

agricultural, urban, mixed (deeper 

aquifers of regional extent in the case of 

ground water), and undeveloped. In this 

action, the NAWQA pesticide data for 

surface water are referenced as Martin et 

al. (2003) and the ground water data are 

referenced as Kolpin and Martin (2003). 

(2) The National Survey of MTBE and 

Other VOCs in Community Drinking 

Water Sources (part of the VOC National 

Synthesis Project). In 2003, USGS 

published the survey findings for 

MTBE, other ether gasoline oxygenates, 

and other volatile organic compounds 

(VOCs) in source water used by CWSs 

in the United States. The survey was 

funded by AWWARF and performed by 

USGS in collaboration with the 

Metropolitan Water District of Southern 

California and the Oregon Health and 

Science University. USGS performed 

the survey in two independent stages 

designed to provide representative 

sampling of all CWSs in the United 

States (Random Source-Water Survey) 

and to improve understanding of the 

temporal variability of MTBE and other 

compounds in selected water sources 

(Focused Source-Water Survey). 

Participating water utilities provided 

samples that were analyzed for 66 

VOCs. The random survey design 

selected 954 CWSs to be nationally 

representative of surface and ground 

waters sources used by CWSs. The 

focused survey studied source waters 

from 134 CWSs suspected or known to 

contain MTBE. The reports/results and 

data sets from the survey can be 

accessed at http://sd.water.usgs.gov/ 

nawqa/vocns/nat—survey.html. The 

random survey results can be found in 

the USGS Water Resources 

Investigations Report 02–4079, 

referenced as Grady (2003). The focused 

survey results can be found in the USGS 

Water Resources Investigations Report 

02–4084, referenced as Delzer and 

Ivahnenko (2003a). 

b. USGS National Highway Runoff 

Data and Methodology Synthesis. In 

addition to the NAWQA project, USGS 

has prepared additional surveys of 

national contaminant occurrence. For 

the National Highway Runoff Data and 

Methodology Synthesis, USGS 

conducted a review of 44 studies of 

semi-volatile organic compounds 

(SVOCs) and VOCs in runoff conducted 

since 1970. The USGS Synthesis sought 

to evaluate data quality parameters for 

comparison between and among these 

studies, including documentation of 

sampling protocols and methods, limits 

of reporting and detection, and 

protocols of quality-control and qualityassurance. The complete USGS report is 

Open-File Report 98–409 and is 

referenced as Lopes and Dionne (1998). 

c. Toxics Release Inventory. EPA 

established the Toxics Release Inventory 

(TRI) in 1987 in response to section 313 

of the Emergency Planning and 

Community Right-to-Know Act 

(EPCRA). EPCRA section 313 requires 

facilities to report to both EPA and the 

States annual information on toxic 

chemical releases from facilities that 

meet reporting criteria. EPCRA section 

313 also requires EPA to make this 

information available to the public 

through a computer database. This 

database is accessible through TRI 

Explorer, which can be accessed at 

http://www.epa.gov/triexplorer. In 1990 

Congress passed the Pollution 

Prevention Act, which required that 

additional data on waste management 

and source reduction activities be 

reported under TRI. The TRI database 

details not only the types and quantities 

of toxic chemicals released to the air, 

water, and land by facilities, but also 

provides information on the quantities 

of chemicals sent to other facilities for 

further management (USEPA, 2002b and 

2003b). 

Facilities are required to report 

releases and other waste management 

activities related to TRI chemicals if 

they manufacture, process, or otherwise 

use more than established threshold 

quantities of these chemicals. Currently 


rmajette on DSK29S0YB1PROD with MISCELLANEOUS
24026 Federal Register / Vol. 72, No. 83 / Tuesday, May 1, 2007 / Proposed Rules 

for most chemicals, the thresholds are 

25,000 pounds for manufacturing and 

processing and 10,000 pounds for use. 

Although TRI can provide a general idea 

of release trends, it is far from 

exhaustive and should not be used to 

estimate general public exposure to a 

chemical (USEPA, 2002b and 2003b). 

d. Pesticides in Ground Water 

Database. The Pesticides in Ground 

Water Database (PGWDB) is a 

compilation of data from ground water 

studies conducted by Federal, State, and 

local governments, the pesticide 

industry, and other institutions between 

1971 and 1991 (USEPA, 1992b). Data 

from 68,824 wells in 45 states are 

included. The vast majority of the wells 

(65,865) were drinking water wells. 

Monitoring was conducted for 258 

pesticides and 45 degradates. Not all 

studies tested for every compound. 

e. The National Pesticide Survey. In 

1990, EPA completed a national survey 

of pesticides in drinking water wells. 

The purpose of the National Pesticide 

Survey (NPS) was to determine the 

national occurrence frequencies and 

concentrations of select pesticides in the 

nation’s drinking water wells, and to 

improve EPA’s understanding of how 

pesticide occurrence in ground water 

correlates with patterns of pesticide 

usage and ground water vulnerability. 

The survey included approximately 

1,300 CWS wells and rural domestic 

wells. Sampling was conducted between 

1988 and 1990. Wells were sampled for 

101 pesticides, 25 pesticide degradates, 

and nitrate. The survey targeted areas 

representing a variety of pesticide usage 

levels and ground water vulnerability. 

The survey was designed to provide a 

statistically reliable estimate of 

pesticide occurrence in the nation’s 

drinking water wells (USEPA, 1990a). 

f. The AWWARF Boron Study. The 

American Water Works Research 

Foundation funded a survey to evaluate 

the occurrence of boron (as well as 

hexavalent chromium) in drinking water 

sources (Frey et al., 2004). The 

AWWARF study recruited 189 PWSs 

representing 407 source waters in 41 

states. Of the 407 source water sample 

kits distributed in 2003, approximately 

342 were returned. Of these 342 

samples, 341 were analyzed for boron. 

Approximately 67 percent (or 228) 

represented ground water sources and 

33 percent (or 113) represented surface 

water sources. The results of the 

AWWARF survey for boron are 

presented in section IV.B of this action. 

3. Supporting Documentation for 

Occurrence. As mentioned in section 

II.E, EPA prepared several technical 

occurrence documents to support this 

action. These technical occurrence 

documents include the following: 

<bullet≤ ‘‘The Analysis of Occurrence 

Data from the Unregulated Contaminant 

Monitoring (UCM) Program and 

National Inorganics and Radionuclides 

Survey (NIRS) in Support of Regulatory 

Determinations for the Second Drinking 

Water Contaminant Candidate List’’ 

(USEPA, 2006c), which this action 

refers to as the ‘‘UCM and NIRS 

Occurrence Report.’’ 

<bullet≤ ‘‘The Analysis of Occurrence 

Data from the First Unregulated 

Contaminant Monitoring Regulation 

(UCMR 1) in Support of Regulatory 

Determinations for the Second Drinking 

Water Contaminant Candidate List’’ 

(USEPA, 2006b), which this action 

refers to as the ‘‘UCMR 1 Occurrence 

Report.’’ 

The ‘‘UCM and NIRS Occurrence 

Report’’ provides more detailed 

information about the UCM and the 

NIRS data, how EPA assessed the data 

quality, completeness, and 

representativeness, and how the data 

were used to generate estimates of 

contaminant occurrence. The ‘‘UCMR 1 

Occurrence Report’’ provides more 

detailed information about the UCMR 1 

data, how EPA assessed the data quality, 

completeness, representativeness, and 

how the data were used to generate 

estimates of contaminant occurrence. 

The comprehensive regulatory 

support document (USEPA, 2006a) 

provides a summary of the results from 

the drinking water occurrence analyses 

discussed in the aforementioned 

technical support documents, as well as 

information on production and use, 

environmental releases, and/or 

occurrence in ambient water, potential 

health effects, the Agency’s preliminary 

determination, and the rationale for the 

determination. 

IV. Preliminary Regulatory 

Determinations 

A. Summary of the Preliminary 

Regulatory Determination 

The Agency has made a preliminary 

determination that each of the 11 

contaminants listed in Table 3 do not 

meet all three of the SDWA criteria 

(discussed in section II.C) and thus do 

not warrant regulation with an NPDWR. 

Table 3 also summarizes the primary 

information used to make these 

regulatory determinations. Section IV.B 

of this action provides a more detailed 

summary of the information and the 

rationale used by the Agency to reach its 

preliminary decisions. The Agency 

solicits public comment on the 

preliminary determinations for these 11 

contaminants. 

BILLING CODE 6560–50–P 


rmajette on DSK29S0YB1PROD with MISCELLANEOUS
Federal Register / Vol. 72, No. 83 / Tuesday, May 1, 2007 / Proposed Rules 24027 

BILLING CODE 6560–50–C 

B. Contaminant Profiles 

This section provides further details 

on the background, health, and 

occurrence information that the Agency 

used to evaluate each of the 11 

candidate contaminants considered for 

regulatory determination. For each 

candidate, the Agency evaluated the 

available human and toxicological data, 

derived a health reference level, and 

evaluated the potential and/or likely 

occurrence and exposed population for 

the contaminant in public water 

systems. The Agency used the findings 

from these evaluations to determine 

whether the three SDWA statutory 

requirements were satisfied. 

As discussed in section II.E, the 

Agency has also prepared a regulatory 

support document (USEPA, 2006a) that 

provides more details on the 

background, health, and occurrence 

information/analyses used to evaluate 

and make preliminary determinations 

for these 11 candidates. 

1. Boron 

a. Background. Boron, a metalloid, 

tends to occur in nature in the form of 

borates (e.g., boric acid, borax, boron 

oxide). Man-made releases are typically 

in the form of borates or boron halides 

(e.g., boron trichloride, boron 

trifluoride). Boron compounds are used 

in the production of glass, ceramics, 

soaps, fire retardants, pesticides, 

cosmetics, photographic materials, and 

high energy fuels (USGS, 2004; ATSDR, 

1992). 

Natural processes such as the 

weathering of rocks, volcanic activity, 

and geothermal steam contribute to the 

release of boron in the environment. 

Releases to the environment from 

human activities occur through the 

production, use, and disposal of boroncontaining compounds (e.g., industrial 

emissions, fertilizer and herbicide 

runoff, hazardous waste deposits, and 

municipal sewage) (HSDB, 2004a; 

ATSDR, 1992). 

Although quantitative data are not 

available on the man-made releases of 

most borates in the United States, two 

boron halide compounds, boron 

trichloride and boron trifluoride, are 

listed as Toxics Release Inventory (TRI) 

chemicals. TRI data for boron 

trichloride and boron trifluoride are 

reported for the years 1995 to 2003 

(USEPA, 2006d). The TRI data show 

boron trichloride releases from facilities 

in 6 States and indicate that air 

emissions account for all of the total 

releases of boron trichloride (on- and 

off-site), which generally fluctuated in 

the range of hundreds of pounds per 

year during the period of record. The 

TRI data show boron trifluoride releases 

from facilities in 14 States and indicate 

that air emissions also account for 

nearly all of the boron trifluoride 

releases, which ranged in the tens of 

thousands of pounds annually. 

b. Health Effects. The Institute of 

Medicine (IOM, 2001) of the National 

Academies categorizes boron as a 

possible trace mineral nutrient for 

humans. Boron is essential for plant 

growth and deficiency studies in 

animals and humans have provided 

some evidence that low intakes of boron 

affects cellular function and the activity 

of other nutrients. It may interact with 

Vitamin D and calcium homeostasis, 

influence estrogen metabolism, and play 

a role in cognitive function (IOM, 2001). 

Iyengar et al. (1988) reported an average 

dietary intake of 1.5 mg/day for male 

adults based on the Food and Drug 

Administration (FDA) Total Diet Study 

(TDS). 

Some human oral data are available 

from cases where boron was ingested as 

a medical treatment. When the amount 

ingested was less than 3.68 mg/kg, 

subjects were asymptomatic, while 

doses of 20 and 25 mg/kg resulted in 

nausea and vomiting. Case reports and 

surveys of accidental poisonings 

indicate that the lethal doses of boron 

range from 15 to 20 grams 

(approximately 200 to 300 mg/kg) for 

adults, 5 to 6 grams (approximately 70 

to 85 mg/kg) for children, and 2 to 3 

grams (approximately 30 to 45 mg/kg) 

for infants (USEPA, 2004b). 

The primary adverse effects seen in 

animals after chronic exposure to low 

doses of boron generally involve the 

testes and developing fetus. Chronic 

effects of dietary boron exposure in twoyear studies included testicular atrophy 

and spermatogenic arrest in dogs, 

decreased food consumption, 


rmajette on DSK29S0YB1PROD with MISCELLANEOUSEP01MY07.051
24028 Federal Register / Vol. 72, No. 83 / Tuesday, May 1, 2007 / Proposed Rules 

suppressed growth, and testicular 

atrophy in rats, and decreased survival, 

testicular atrophy, and interstitial cell 

hyperplasia in mice. Although 

researchers observed some increases in 

tumor incidences in the liver and in 

subcutaneous tissues in mice, based on 

comparisons to historic controls, these 

tumors were determined not to be 

associated with exposure to boron from 

boric acid (USEPA, 2004b). Boron is not 

considered mutagenic and the Agency 

determined that there are inadequate 

data to assess the human carcinogenic 

potential for boron (USEPA, 2004c). 

In developmental studies with rats, 

mice, and rabbits, oral exposure to boric 

acid resulted in decreased pregnancy 

rate, increased prenatal mortality, 

decreased fetal weights, and increased 

malformations in fetuses and pups. 

However, these reproductive effects 

were associated with maternal toxicity 

including changes in maternal organ 

weights, body weights, weight gain, and 

increased renal tubular dilation and/or 

regeneration (Price et al., 1990, 1994, 

1996; Heindel et al., 1992, 1994; Field 

et al., 1989). Reproductive effects in 

males were noted in the subchronic and 

chronic studies described in the 

preceding paragraphs. 

The EPA RfD for boron is 0.2 mg/kg/ 

day (USEPA, 2004c) based on 

developmental effects in rats from two 

studies (Price et al., 1996; Heindel et al., 

1992). The RfD was derived using the 

benchmark dose (BMD) method (bench 

mark dose level or BMDL from Allen et 

al., 1996). EPA calculated the HRL of 

1.4 mg/L or 1,400 [mu]g/L for boron 

using the RfD of 0.2 mg/kg-day and a 20 

percent screening relative source 

contribution. 

EPA also evaluated whether health 

information is available regarding the 

potential effects on children and other 

sensitive populations. Studies in rats, 

mice, and rabbits identify the 

developing fetus as potentially sensitive 

to boron. Price et al. (1996) identified a 

LOAEL of 13.3 mg/kg-day and an 

NOAEL of 9.6 mg/kg-day in the 

developing fetus, based on decreased 

fetal body weight in rats. Accordingly, 

boron at concentrations greater than the 

HRL might have an effect on prenatal 

development. Individuals with severely 

impaired kidney function might also be 

sensitive to boron exposure since the 

kidney is the most important route for 

excretion. 

c. Occurrence Analyses. The National 

Inorganics and Radionuclides Survey 

(NIRS) included boron as an analyte. 

Using data from NIRS, EPA performed 

an initial evaluation of occurrence and 

exposure at levels greater than 700 

[mu]g/L (1⁄2 the HRL) and greater than 

1,400 [mu]g/L (the HRL for boron). The 

NIRS data indicate that approximately 

4.3 percent (or 43) of the 989 ground 

water PWSs sampled had detections of 

boron at levels greater than 700 [mu]g/ 

L, affecting approximately 2.9 percent of 

the population served (or 42,700 people 

from 1.48 million). Approximately 1.7 

percent (or 17) of 989 ground water 

PWSs sampled had detections of boron 

at levels greater than 1,400 [mu]g/L, 

affecting approximately 0.4 percent of 

the population served (6,400 people 

from 1.48 million) (USEPA, 2006a and 

2006c). 

Because NIRS did not contain data for 

surface water systems, the Agency 

evaluated the results of a survey funded 

by the American Water Works 

Association Research Foundation (Frey 

et al., 2004) to gain a better 

understanding of the potential 

occurrence of boron in surface water 

systems. The AWWARF study recruited 

189 PWSs representing 407 source 

waters that covered 41 states. Of these 

407 PWS source water samples, 342 

were returned and 341 were analyzed 

for boron. Of these 341 samples, 

approximately 67 percent (or 228) 

represented ground water sources and 

33 percent (or 113) represented surface 

water sources. None of the 113 surface 

water sources exceeded the boron HRL 

of 1,400 [mu]g/L and the maximum 

concentration observed in surface water 

was 345 [mu]g/L. Extrapolation of the 

data indicates that 95 percent of the 

ground water detections had boron 

levels less than 1,054 [mu]g/L; the 

maximum observed concentration in 

ground water was approximately 3,300 

[mu]g/L. Seven of the 228 ground water 

sources (from 5 systems) had boron 

concentrations greater than 1,400 [mu]g/ 

L (Seidel, 2006). 

d. Preliminary Determination. The 

Agency has made a preliminary 

determination not to regulate boron 

with an NPDWR. While boron was 

found at levels greater than the HRL 

(and 1⁄2 the HRL) in several of the 

ground water systems surveyed by 

NIRS, it was not found at levels greater 

than the HRL (or 1⁄2 the HRL) in the 

surface waters sources evaluated in the 

AWWARF study. Taking this surface 

water information into account, the 

Agency believes that the overall 

national occurrence and exposure from 

both surface and ground water systems 

together is likely to be lower than the 

values observed for the NIRS ground 

water data. Because boron is not likely 

to occur at levels of concern when 

considering both surface and ground 

waters systems, the Agency believes that 

a national primary drinking water 

regulation does not present a 

meaningful opportunity for health risk 

reduction. 

The Agency encourages those States 

with public water systems that have 

boron at concentrations above the HRL 

to evaluate site-specific protective 

measures and to consider whether Statelevel guidance (or some other type of 

action) is appropriate. The Agency also 

plans to update the Health Advisory for 

boron to provide more recent health 

information. The updated Health 

Advisory will provide information to 

any States with public water systems 

that may have boron above the HRL. 

2 and 3. Mono- and Di-Acid Degradates 

of Dimethyl Tetrachloroterephthalate 

(DCPA) 

a. Background. Dimethyl 

tetrachloroterephthalate (DCPA), a 

synthetic organic compound (SOC) 

marketed under the trade name 

‘‘Dacthal,’’ is a pre-emergent herbicide 

historically used to control weeds in 

ornamental turf and plants, 

strawberries, seeded and transplanted 

vegetables, cotton, and field beans. As of 

1990, more than 80 percent of its use 

was for turf, including golf courses and 

home lawns (USEPA, 1990b). On July 

27, 2005, in response to concerns about 

groundwater contamination (especially 

for one of the DCPA degradates), the 

Agency published a Federal Register 

notice announcing that the registrant for 

Dacthal had voluntarily terminated a 

number of uses for products containing 

DCPA (70 FR 43408; USEPA, 2005f). 

The only uses retained were those for 

use on sweet potatoes, eggplant, kale 

and turnips. 

DCPA is not especially mobile or 

persistent in the environment. 

Biodegradation and volatilization are 

the primary dissipation routes. 

Degradation of DCPA forms two 

breakdown products, the mono-acid 

degradate (or monomethyl 

tetrachloroterephthalate or MTP) and 

the di-acid degradate 

(tetrachloroterephthalic acid or TPA). 

The di-acid, which is the major 

degradate, is unusually mobile and 

persistent in the field, with a potential 

to leach into water (USEPA, 1998c). 

Several studies and reports provide 

estimates of the amount of DCPA used 

during the 1990s in the United States. 

The Agency estimated that 1.6 million 

pounds of DCPA active ingredient a.i. 

were used annually in the early 1990s 

(USEPA, 1998c). USGS estimated that 

approximately 998 thousand pounds of 

DCPA a.i. were used annually circa 

1992 (Thelin and Gianessi, 2000). The 

National Center for Food and 

Agricultural Policy (NCFAP, 2004) 

estimates that approximately 1.7 million 


rmajette on DSK29S0YB1PROD with MISCELLANEOUS
Federal Register / Vol. 72, No. 83 / Tuesday, May 1, 2007 / Proposed Rules 24029 

pounds of DCPA a.i. were used in 1992 

and approximately 600 thousand 

pounds a.i. were used in 1997 (NCFAP, 

2004). The NCFAP data suggest a 

decrease in the use of DCPA from the 

early to the late 1990s. b. Health Effects. Currently, no 

subchronic or chronic studies are 

available to assess the toxicological 

effects of MTP (the mono-acid 

degradate) and 3 studies in rats (30 and 

90-day feeding studies and a onegeneration reproductive study) are 

available for TPA (the di-acid 

degradate). The effects of exposure were 

mild (weight loss and diarrhea) and 

occurred at doses greater than or equal 

to 2,000 mg/kg/day. No reproductive 

effects were observed. 

The present toxicity database for MTP 

and TPA is not sufficient to derive RfDs 

for these two chemicals. However, since 

the available data indicate that neither 

MTP nor TPA are more toxic than their 

parent compound, DCPA, the Agency 

suggests that the RfD for the DCPA 

parent would be protective against 

exposure from these two DCPA 

metabolites (USEPA, 1998c). Both 

compounds are formed in the body from 

the DCPA parent and therefore, the 

toxicity of these degradates is reflected 

in the toxicity of the parent. The RfD for 

DCPA is 0.01 mg/kg/day based on a 

chronic rat study (ISK Biotech 

Corporation, 1993) with a NOAEL of 1.0 

mg/kg/day and an uncertainty factor of 

100 for rat to human extrapolation and 

intra-species variability. No carcinogenicity studies have been 

performed using either TPA or MTP. 

Based on the cancer data for the parent 

and lack of mutagenicity for TPA and 

DCPA, the Agency (USEPA, 2004d) 

concludes that TPA is unlikely to pose 

a cancer risk. Klopman et al. (1996) 

evaluated the carcinogenic potential of 

TPA based on its chemical and 

biological properties, as well as by a 

variety of computational tools, and 

determined that it did not present any 

substantial carcinogenic risk. There was 

suggestive evidence that DCPA could be 

carcinogenic based on an increased 

incidence of thyroid and liver tumors in 

rats. The presence of hexachlorobenzene 

and dioxin as impurities in the material 

tested could have contributed to the 

cancer risk. 

Using the DCPA RfD of 0.01 mg/kg/ 

day (USEPA, 1994) and a 20 percent 

screening relative source contribution, 

the Agency calculated an HRL of 0.07 

mg/L or 70 [mu]g/L for DCPA and used 

this HRL for TPA and MTP. 

EPA also evaluated whether health 

information is available regarding the 

potential effects on children and other 

sensitive populations. There are no data 

that identify a particular sensitive 

population for DCPA exposure. Results 

of a single developmental study indicate 

that exposure to pregnant dams with 

doses less than or equal to 2,500 mg/kg/ 

day of TPA via gavage did not have an 

adverse effect on the fetus. EPA did not 

identify any data that suggest genderrelated differences in toxicity or 

sensitivity in the elderly. c. Occurrence. EPA included the 

DCPA mono- and di-acid degradates 

(MTP and TPA) as analytes in the 

UCMR 1. The analysis results reported 

for UCMR 1 are the sum of both the 

mono- and di-acid degradates. EPA 

converted the analysis result for the 

degradates to the parent DCPA 

equivalent and performed an initial 

evaluation of occurrence and exposure 

at levels greater than 35 [mu]g/L (1⁄2 the 

HRL) and greater than 70 [mu]g/L (the 

HRL). As previously discussed, EPA 

used the HRL derived for the DCPA 

parent because it includes the toxicity 

for the mono- and di-acid degradates. 

While the UCMR 1 data indicate that the 

DCPA degradates were the most 

commonly reported analytes in the 

monitoring survey (detected at an MRL 

of 1 [mu]g/L in 772 samples from 175 

of the 3,868 PWSs sampled), very few 

systems exceeded the health level of 

concern. PWSs with detections were 

found in 24 States and 1 Territory. The 

UCMR 1 data indicate that 

approximately 0.05 percent (or 2) of the 

3,868 PWSs sampled had a detection of 

the DCPA degradates at levels greater 

than 35 [mu]g/L, affecting 

approximately 0.33 percent of the 

population served (or 739,000 people 

from 225 million). Approximately 0.03 

percent (or 1) of the 3,868 PWSs 

sampled have a detection of the DCPA 

degradates at levels greater than 70 

[mu]g/L, affecting less than 0.01 percent 

of the population served (or 500 people 

from 225 million) (USEPA, 2006a and 

2006b). 

EPA also evaluated several sources of 

supplemental occurrence information 

for the DCPA parent, the mono-acid 

degradate and/or the di-acid degradate. 

These supplemental sources include: <bullet≤ The National Pesticide 

Survey (NPS), <bullet≤ The provisional pesticide 

results from the 1992–2001 USGS 

NAWQA survey of ambient surface and 

ground waters across the U.S., and <bullet≤ Studies performed by the 

DCPA or dacthal registrant. As part of the National Pesticide 

Survey, EPA collected samples from 

approximately 1,300 community water 

systems and rural drinking water wells 

between 1988 and 1990. The NPS 

included monitoring for the DCPA 

parent and the di-acid degradate. The 

DCPA parent was not detected in any 

wells (using a detection limit of 0.06 

[mu]g/L). While the di-acid degradate 

was detected in 49 of 1,347 wells (using 

a detection limit of 0.1 [mu]g/L), the 

maximum reported concentration of 7.2 

[mu]g/L did not exceed the HRL of 70 

[mu]g/L (USEPA, 1990a). 

The USGS NAWQA program included 

the DCPA parent and the mono-acid 

degradate as analytes in its 1992–2001 

monitoring survey of ambient surface 

and ground waters across the United 

States. EPA evaluated the results of the 

provisional data, which are available on 

the Web (Martin et al., 2003; Kolpin and 

Martin, 2003). While the USGS detected 

the DCPA parent in both surface and 

ground waters, at least 95 percent of the 

samples from the various land use 

settings were less than or equal to 0.007 

[mu]g/L. The estimated maximum 

surface water concentration, 40 [mu]g/L 

(agricultural setting), and the estimated 

maximum ground water concentration, 

10 [mu]g/L (agricultural setting), are 

both less than 70 [mu]g/L (the DCPA 

HRL). While the USGS detected the 

mono-acid degradate in both surface 

waters and ground waters, at least 95 

percent of the samples from the various 

land use settings were less than 0.07 

[mu]g/L (the reporting limit for the 

mono-acid degradate). The maximum 

surface water concentration, 0.43 [mu]g/ 

L (agricultural setting), and the 

maximum ground water concentration, 

1.1 [mu]g/L (agricultural setting), are 

both less than 70 [mu]g/L (the DCPA 

HRL, which includes the toxicity of the 

degradates). 

Beginning in 1992, the registrant for 

DCPA performed two small-scale 

ground water occurrence studies in New 

York and California over a period of 17 

and 22 months, respectively. The 

registrant monitored for the DCPA 

parent and both of its degradates. The 

average reported values, which are the 

sum of the parent and its degradates, 

were 50.36 [mu]g/L in New York and 

12.75 [mu]g/L in California. Neither 

average value exceeded the HRL of 70 

[mu]g/L (USEPA, 1998c). 

d. Preliminary Determination. The 

Agency has made a preliminary 

determination not to regulate the DCPA 

mono-acid degradate and/or the DCPA 

di-acid degradate with an NPDWR. 

Because these degradates appear to 

occur infrequently at health levels of 

concern in PWSs, the Agency believes 

that a national primary drinking water 

regulation does not present a 

meaningful opportunity for health risk 

reduction. While the Agency recognizes 

that these degradates have been detected 

in the PWSs monitored under the 

UCMR 1, only 1 PWS had a detect above 

the HRL. 


rmajette on DSK29S0YB1PROD with MISCELLANEOUS
24030 Federal Register / Vol. 72, No. 83 / Tuesday, May 1, 2007 / Proposed Rules 

15 1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane. 

16 Karst is a type of typography that is formed by 

the dissolution and collapse of soluble rocks 

(typically limestone and dolomite). According to 

the Karst Waters Institute, as excerpted by USGS 

(2006), common geological characteristics of karst 

regions that influence human use of its land and 

water resources include ground subsidence, 

The Agency encourages those States 

with public water systems that have 

detects for these degradates to evaluate 

site-specific protective measures and to 

consider whether State-level guidance 

(or some other type of action) is 

appropriate. The Agency also plans to 

update the Health Advisory for the 

DCPA parent to include the mono and 

di acid degradates, as well as any recent 

health information related to these 

compounds. The updated Health 

Advisory will provide information to 

any States with public water systems 

that may have DCPA degradates at 

levels above the HRL. 

4. 1,1-Dichloro-2,2-bis(p-chlorophenyl) 

ethylene (DDE) 

a. Background. DDE is a primary 

metabolite of DDT,15 a pesticide once 

used to protect crops and eliminate 

disease-carrying insects in the U.S. until 

it was banned in 1973. DDE itself has no 

commercial use and is only found in the 

environment as a result of 

contamination and/or breakdown of 

DDT. While DDE tends to adsorb 

strongly to surface soil and is fairly 

insoluble in water, it may enter surface 

waters from runoff that contains soil 

particles contaminated with DDE. In 

both soil and water, DDE is subject to 

photodegradation, biodegradation, and 

volatilization (ATSDR, 2002). 

b. Health Effects. DDE is not produced 

as a commercial product. This has 

limited the numbers of conventional 

studies that have been performed to 

assess toxicological properties. Limited 

data on DDE, mostly from a National 

Cancer Institute (NCI) bioassay, suggest 

that the liver is the primary target organ 

in mammalian species. However, the 

NCI study did not evaluate a full array 

of noncancer endpoints. There is an RfD 

of 0.0005 mg/kg/day for the parent 

pesticide DDT based on a NOAEL of 

0.05 mg/kg/day from a dietary 

subchronic study (USEPA, 1996b). In 

this study, liver lesions were identified 

at a LOAEL of 0.25 mg/kg/day. Data on 

DDT identify effects on the nervous and 

hormonal systems as adverse effects that 

might also be seen with DDE because it 

is one of DDT’s primary metabolites. 

The limited data for DDE suggest that 

any effects on the nervous system are 

less severe than those seen with DDT. 

Endocrine effects from DDE are 

discussed in this section. 

Based on animal studies DDE is likely 

to be carcinogenic to humans. This 

classification is based on increases in 

the incidence of liver tumors, including 

carcinomas, in two strains of mice and 

in hamsters after dietary exposure to 

DDE. Some epidemiological studies 

suggest a possible association of the 

levels of DDE in serum with breast 

cancer. However, other studies with 

similar methodologies do not show any 

association. DDE was mutagenic in 

mouse lymphoma L5178Y and Chinese 

hamster V79 cells but negative in the 

Ames assay. In the 1988 IRIS, EPA 

calculated an oral slope factor of 0.34 

(mg/kg/day)-1 for DDE (USEPA, 1988a). 

For this regulatory determination, EPA 

calculated an oral slope factor from the 

same data set (from the 1988 IRIS) using 

the EPA 1999 Cancer Guidelines 

(USEPA, 1999a). The revised slope 

factor is 1.67 x 10-1 (mg/kg/day)-1

resulting in a one-in-a-million cancerrisk (HRL) of 0.2 [mu]g/L. There are some indications that DDE 

has an adverse impact on the immune 

system (Banerjee et al., 1996). Oral 

exposures to 22 mg/kg/day for 6 weeks 

suppressed serum immunoglobin levels 

and antibody titers. Inhibition of 

leucocytes and macrophage migration 

were observed at the cellular level. 

Considerable evidence exists that DDE 

can act as an endocrine disruptor since 

it binds to the estrogen and androgen 

receptors. DDE has a stronger affinity for 

the androgen receptor than for the 

estrogen receptor. It competes with 

testicular hormones for the androgen 

receptor leading to receptor-related 

changes in gene expression (Kelce et al., 

1995). 

EPA evaluated whether health 

information is available regarding the 

potential effects on children and other 

sensitive populations. Children and 

adolescents may be sensitive 

populations for exposure to DDE due to 

its endocrine disruption properties. 

Some data suggest that DDE can delay 

puberty in males (ATSDR, 2002). c. Occurrence. EPA included DDE as 

an analyte in the UCMR 1. Because the 

HRL for DDE (0.2 [mu]g/L) is lower than 

the minimum reporting limit (MRL) 

used for monitoring (0.8 [mu]g/L), EPA 

used the MRL value to evaluate 

occurrence and exposure. The MRL is 

within the 10-4 to the 10-6 cancer risk 

range for DDE. In evaluating the UCMR 

1 data, EPA found that approximately 

0.03 percent (or 1) of the 3,867 PWSs 

sampled had a detection of DDE at the 

MRL of 0.8 [mu]g/L, affecting 

approximately 0.01 percent of the 

population served (or 18,000 people 

from 226 million) (USEPA, 2006a and 

2006b). 

The USGS NAWQA program included 

DDE as an analyte in its 1992–2001 

monitoring survey of ambient surface 

and ground waters across the United 

States. EPA evaluated the results of the 

provisional data, which are available on 

the Web (Martin et al., 2003; Kolpin and 

Martin, 2003), as a supplemental source 

of occurrence information. While the 

USGS detected DDE in both surface and 

ground waters, 95 percent of the 

samples from the various land use 

settings were less than 0.006 [mu]g/L 

(the USGS reporting limit). The 

maximum surface water concentration, 

0.062 [mu]g/L (agricultural setting), and 

the maximum ground water 

concentration, 0.008 [mu]g/L 

(agricultural setting), are both less than 

0.2 [mu]g/L (the DDE HRL). d. Preliminary Determination. The 

Agency has made a preliminary 

determination not to regulate DDE with 

an NPDWR. Because DDE appears to 

occur infrequently at levels of concern 

in PWSs, the Agency believes that a 

national primary drinking water 

regulation does not present a 

meaningful opportunity for health risk 

reduction. DDE was detected in only 

one of the PWSs monitored under the 

UCMR 1 at a level greater than the MRL 

(0.8 [mu]g/L), a concentration that is 

within the 10-4 to the 10-6 cancer risk 

range. In addition, ambient water data 

from the USGS indicate that the 

maximum concentrations detected in 

surface and ground water were less than 

the HRL of 0.2 [mu]g/L. EPA recognizes that DDE is listed as 

a probable human carcinogen. For this 

reason, the Agency encourages those 

States with public water systems that 

might have DDE above the HRL to 

evaluate site-specific protective 

measures and to consider whether Statelevel guidance (or some other type of 

action) is appropriate. 

5. 1,3-Dichloropropene (1,3-DCP; 

Telone) 

a. Background. 1,3-Dichloropropene 

(1,3-DCP), a synthetic volatile organic 

compound, is used as a pre-plant soil 

fumigant to control nematodes and 

other pests in soils to be planted with 

all types of food and feed crops. 1,3-DCP 

is typically injected 12’’ to 18’’ beneath 

the soil surface and can only be used by 

certified handlers (USEPA, 1998b). To 

mitigate risks to drinking water, 1999 

labeling requirements restrict the use of 

1,3-DCP: 

<bullet≤ In areas with shallow ground 

water and vulnerable soils in certain 

northern tier States (ND, SD, WI, MN, 

NY, ME, NH, VT, MA, UT, and MT); 

<bullet≤ In fields within 100 feet of a 

drinking water well; and <bullet≤ In areas overlying karst 16

geology. 


rmajette on DSK29S0YB1PROD with MISCELLANEOUS
Federal Register / Vol. 72, No. 83 / Tuesday, May 1, 2007 / Proposed Rules 24031 

sinkhole collapse, ground water contamination, and 

unpredictable water supply. 

Estimates of national annual use 

during the 1990s vary widely, from 

approximately 23 to 40 million pounds 

of active ingredient a.i. Based on 

information from a 1991 data call-in and 

other sources, EPA estimates that 

approximately 23 million pounds of 1,3- 

DCP a.i. were used annually from 1990 

to 1995 (USEPA, 1998b). NCFAP (2004) 

estimates that approximately 40 million 

pounds a.i. were used in 1992 and 

approximately 35 million pounds a.i. 

were used in 1997. 

1,3-Dichloropropene is listed as a TRI 

chemical and releases are reported from 

facilities in 17 States over a time period 

covering 1988 to 2003 (although not all 

States had facilities reporting releases 

every year) (USEPA, 2006e). Air 

emissions appear to account for most of 

the on-site (and total) releases and 

generally declined between 1988 and 

2003. A sharp decrease in air emissions 

is evident between 1995 and 1996. 

Surface water discharges are minor 

compared to air emissions and no 

obvious trend is evident between 1988 

and 2003. Reported underground 

injection, releases to land, and off-site 

releases are generally insignificant. 

b. Health Effects. Chronic and 

subchronic exposures to 1,3-DCP at 

doses of 12.5 mg/kg/day and above in 

animal dietary studies indicate that 1,3- 

DCP is toxic to organs involved in 

metabolism (liver), excretion of 

conjugated metabolites (e.g., urinary 

bladder and the kidney) and organs 

along the portals of entry (e.g., 

forestomach for oral administration; 

mucous membrane of the nasal passage 

and lungs for inhalation exposure). 

Exposure to 1,3-DCP has not been 

shown to cause reproductive or 

developmental effects. Neither 

reproductive nor developmental toxicity 

were observed in a two-generation 

reproductive study in rats or in 

developmental studies in rats and 

rabbits at maternal inhalation 

concentrations up to 376 mg/m3

(USEPA, 2000a). Even concentrations 

that produced parental toxicity did not 

produce reproductive or developmental 

effects (USEPA, 2000a). 

An RfD of 0.03 mg/kg/day for 1,3-DCP 

(USEPA, 2000a) has been established 

using a benchmark dose (BMD) analysis 

based on a two-year chronic bioassay 

(Stott et al., 1995) in which chronic 

irritation (forestomach hyperplasia) and 

significant body weight reduction were 

the critical and co-critical effects, 

respectively. A reference concentration 

(RfC) of 0.02 mg/m3 was derived from a 

two-year bioassay (Lomax et al., 1989), 

which observed histopathology in the 

nasal epithelium. 

Under the proposed cancer risk 

assessment guidelines, the weight of 

evidence for evaluation of 1,3-DCP’s 

ability to cause cancer suggest that it is 

likely to be carcinogenic to humans 

(USEPA, 2000a). This characterization is 

supported by tumor observations in 

chronic animal bioassays for both 

inhalation and oral routes of exposure. The oral cancer slope factors 

calculated from chronic dietary, gavage 

and inhalation data ranged from 5 x 10-2

to 1 x 10-1 (mg/kg/day)-1. Due to 

uncertainties in the delivered doses in 

some studies, EPA (IRIS) recommended 

using the oral slope factor of 1 x 10-1

(mg/kg/day)-1 from an NTP (1985) study. 

Using this oral slope factor, EPA 

calculated an HRL of 0.4 [mu]g/L at the 

10-6 cancer risk level. 

EPA also evaluated whether health 

information is available regarding the 

potential effects on children and other 

sensitive populations. No human or 

animal studies are available that have 

examined the effect of 1,3-DCP exposure 

on juvenile subjects. Therefore, its 

effects on children are unknown. 

Developmental studies in rats and 

rabbits show no evidence of 

developmental effects and therefore it is 

unlikely that 1,3-DCP causes 

developmental toxicity. c. Occurrence. EPA included 1,3-DCP 

as an analyte in the UCM Round 1 and 

UCM Round 2 surveys. The MRLs for 

UCM Round 1 ranged from 0.02 to 10 

[mu]g/L and the MRLs for UCM Round 

2 ranged from 0.08 to 1 [mu]g/L. EPA 

also analyzed for 1,3-DCP using the 

samples from the small systems that 

were included in the UCMR 1 survey. 

The MRL used for the UCMR 1 survey 

was 0.5 [mu]g/L. Because some of these 

reporting limits exceeded the thresholds 

of interest, the occurrence analyses may 

result in an underestimate of systems 

affected (USEPA, 2006a, 2006b and 

2006c). However, the MRL values used 

for UCM Round 1 and UCM Round 2 as 

well as UCMR 1 are within the 10-4 to 

the 10-6 cancer risk range. The UCM Round 1 Cross Section data 

indicate that approximately 0.16 percent 

(or 15) of the 9,164 PWSs sampled had 

detections of 1,3-DCP at levels greater 

than 0.2 [mu]g/L (1⁄2 the HRL), affecting 

approximately 0.86 percent of the 

population served (or 438,000 of 51 

million). The UCM Round 1 Cross 

Section data also indicate the same 

values when the data are analyzed using 

0.4 [mu]g/L (the HRL). That is, 0.16 

percent (or 15) of 9,164 PWSs sampled 

had detections greater than 0.4 [mu]g/L 

(the HRL), affecting approximately 0.86 

percent of the population served (or 

438,000 of 51 million people). The 99th 

percentile of all detections is 2 [mu]g/ 

L and the maximum reported value is 2 

[mu]g/L. 

The UCM Round 2 Cross Section data 

indicate that approximately 0.30 percent 

(or 50) of the 16,787 PWSs sampled had 

detections of 1,3-DCP at levels greater 

than 0.2 [mu]g/L (1⁄2 the HRL), affecting 

approximately 0.42 percent of the 

population served (or 193,000 of 46 

million). The UCM Round 2 Cross 

Section data indicate that approximately 

0.23 percent (or 38) of the 16,787 PWSs 

sampled had detections of 1,3-DCP at 

levels greater than 0.4 [mu]g/L (the 

HRL), affecting approximately 0.33 

percent of the population served (or 

152,000 of 46 million). The 99th 

percentile of all detections is 39 [mu]g/ 

L and the maximum reported value is 39 

[mu]g/L. 

Because the sample preservative used 

may have resulted in potential 

underestimates of occurrence for the 

UCM Rounds 1 and 2 data, EPA 

subsequently analyzed for 1,3-DCP 

using the samples provided by 796 of 

the small systems included in the recent 

UCMR 1 survey. None of the 3,719 

samples from these 796 small systems 

(serving a population of 2.8 million) had 

detects of 1,3-DCP at levels greater than 

0.5 [mu]g/L (the minimum reporting 

limit used for the analysis of 1,3-DCP 

and a level that is slightly higher than 

the HRL). 

EPA also evaluated several sources of 

supplemental information, which 

included: 

<bullet≤ The National Pesticide 

Survey, 

<bullet≤ The Pesticides in Ground 

Water Database, 

<bullet≤ A well water survey 

submitted by the registrant of Telone 

(1,3-DCP), 

<bullet≤ The USGS VOC National 

Synthesis Random Source Water 

Survey, and 

<bullet≤ The USGS VOC National 

Synthesis Focused Source Water 

Survey. 

As part of the National Pesticide 

Survey, EPA collected samples from 

approximately 1,300 community water 

systems and rural drinking water wells 

between 1988 and 1990. The NPS 

included cis and trans 1,3-DCP as 

analytes in the monitoring survey. 

Neither compound was detected in the 

survey using a minimum reporting limit 

of 0.010 [mu]g/L (USEPA, 1990a). 

The Pesticides in Ground Water 

Database (USEPA, 1992b) indicates that 

1,3-DCP was found in 6 of 21,270 

ground water wells sampled in 7 States. 

The 6 wells with positive detections for 

1,3-DCP included 3 wells in California 

(at concentrations ranging from 0.890 to 

31.0 [mu]g/L), 2 wells in Florida (at 

concentrations of 0.279 to 7.83 [mu]g/L), 

and 1 well in Montana (at 

concentrations of 18 to 140 [mu]g/L). 

While most or all of these 6 wells had 


rmajette on DSK29S0YB1PROD with MISCELLANEOUS
24032 Federal Register / Vol. 72, No. 83 / Tuesday, May 1, 2007 / Proposed Rules 

17 LD50 = An estimate of a single dose that is 

expected to cause the death of 50% of the exposed 

animals. It is derived from experimental data. 

concentrations greater than the HRL for 

1,3-DCP, the overall percentage of 

positive wells detections was less than 

0.1 percent. 

In 1998, the registrant for Telone (1,3- 

DCP) submitted a private well water 

study to the Agency. The well water 

survey covered 5 regions where Telone 

was used intensively and evaluated 518 

wells (5,800 samples) for the presence 

of 1,3-DCP. Of the 518 wells, 65 had 

detectable levels of 1,3-DCP and/or its 

metabolites at levels greater than 0.015 

[mu]g/L (the detection limit for 1,3-DCP 

was 0.015 [mu]g/L and the metabolites 

were 0.023 [mu]g/L). None of the wells 

exceeded 0.2 [mu]g/L (a level half the 

EPA-derived HRL for 1,3-DCP) (USEPA, 

2004e and 2004f). 

For the Random Source Water Survey, 

the USGS collected samples from 954 

source waters that supply community 

water systems between 1999 and 2000. 

For the Focused Source Water Survey, 

the USGS collected 451 samples from 

134 source waters that supply 

community water systems between 1999 

and 2001. The USGS included 1,3-DCP 

as an analyte in both surveys. The USGS 

did not detect 1,3-DCP in any of the 

source water samples from the Random 

Source Water Survey using a reporting 

limit of 0.2 [mu]g/L (a level that is onehalf the HRL for 1,3-DCP). In addition, 

the USGS did not detect 1,3-DCP in any 

of the source water samples in the 

Focused Source Water Survey using a 

detection limit of 0.024 [mu]g/L for cis1,3-dichloropropene and 0.026 [mu]g/L 

for trans-1,3-dichloropropene (levels 

that are about 16 times lower than the 

HRL for 1,3-DCP) (Ivahnenko et al., 

2001; Grady, 2003; Delzer and 

Ivahnenko, 2003a). 

d. Preliminary Determination. The 

Agency has made a preliminary 

determination not to regulate 1,3-DCP 

with an NPDWR. Because 1,3-DCP 

appears to occur infrequently at health 

levels of concern in PWSs, the Agency 

believes that a national primary 

drinking water regulation does not 

present a meaningful opportunity for 

health risk reduction. While 1,3-DCP 

was detected in the UCM Round 1 (late 

1980s) and the UCM Round 2 (mid 

1990s) surveys, it was not detected in a 

subsequent evaluation of 796 small 

systems from the UCMR 1 survey. In 

addition, the USGS did not detect 1,3- 

DCP in two occurrence studies 

performed between 1999 and 2001 using 

monitoring levels that were lower than 

the HRL. EPA believes the 1999 

pesticide labeling requirements, which 

are intended to mitigate risks to 

drinking water, may be one reason for 

the lack of occurrence of 1,3-DCP at 

levels of concern in subsequent 

monitoring surveys. 

EPA recognizes that 1,3- 

dichloropropene is listed as a probable 

human carcinogen. For this reason, the 

Agency encourages those States with 

public water systems that may have 1,3- 

dichloropropene above the HRL to 

evaluate site-specific protective 

measures and to consider whether Statelevel (or some other type of action) is 

appropriate. The Agency also plans to 

update the Health Advisory document 

for 1,3-DCP to provide more recent 

health information. The updated Health 

Advisory will provide information to 

any States with public water systems 

that may have 1,3-DCP above the HRL. 

6 and 7. 2,4- and 2,6-Dinitrotoluenes 

(2,4- and 2,6-DNT) 

a. Background. 2,4- and 2,6- 

dinitrotoluene (DNT), semi-volatile 

organic compounds, are two of 6 

isomers of dinitrotoluene. 

Dinitrotoluenes are used in the 

production of polyurethane foams, 

automobile air bags, dyes, ammunition, 

and explosives, including 

trinitrotoluene or TNT (HSDB, 2004b 

and 2004c; ATSDR, 1998). Neither 2,4- 

nor 2,6-DNT occur naturally. They are 

generally produced as individual 

isomers or as a mixture called technical 

grade DNT (tg-DNT). Technical grade 

DNT primarily contains a mixture of 

2,4-DNT and 2,6-DNT with the 

remainder consisting of the other 

isomers and minor contaminants such 

as TNT and mononitrotoluenes (HSDB, 

2004b). 

No recent quantitative estimates of 

DNT production or use are available. 

The Hazardous Substances Data Bank 

(HSDB, 2004b) cites a 1980 EPA 

Ambient Water Quality Criteria 

Document that places combined 2,4- 

and 2,6-DNT production at 272,610,000 

pounds in 1975. 

Both 2,4-DNT and 2,6-DNT are listed 

as TRI chemicals. TRI data for 2,4-DNT 

are reported from facilities in 21 States 

over a time period covering 1988 to 

2003. Total releases nationally in 2003 

were 14,899 lbs. Releases of all kinds 

(off-site releases and on-site air, surface, 

underground injection, and land 

releases) declined in the early 1990s, 

and then peaked again around 1999– 

2001. On-site air emissions and surface 

water releases of 2,4-DNT were 

generally the most consistent (least 

fluctuating) types of releases, with 

surface water releases generally 

declining over the period on record 

(USEPA, 2006f). 

TRI data for 2,6-DNT are reported 

from facilities in 10 States over a time 

period covering 1988 to 2003 (with no 

more than 9 States having reporting 

facilities in any one year). Total 

reported releases for 2003 were 10,937 

lbs. Trends for 2,6-DNT are similar to 

those for 2,4-DNT. The TRI data for 2,6- 

DNT show a trend of declining releases 

in the late 1980s and early 1990s, and 

a subsequent peak around 1999–2001. 

On-site air emissions and surface water 

discharges are the most consistent types 

of release for 2,6-DNT and surface water 

discharges exhibit a declining trend 

(USEPA, 2006f). 

In addition, TRI lists mixed DNT 

isomer releases as a separate category 

over the same time period (1990–2003). 

TRI releases of mixed isomers were 

reported from facilities in 9 States, with 

no more than 7 States having reporting 

facilities in any one year. Total releases 

in 2003 were 13,790 lbs. Underground 

injections made up the bulk of on-site 

releases during the 1990s, but 

diminished thereafter. Air emissions 

remained relatively constant. Surface 

water discharges and releases to land 

were generally insignificant but peaked 

in 2003. Off-site releases varied widely. 

Total releases peaked in 1993 and 1997, 

and generally diminished in recent 

years (USEPA, 2006f). 

b. Health Effects. In experimental 

animal studies, 2,4- and 2,6-DNT appear 

to be acutely toxic at moderate to high 

levels (LD50’s 17 ranging from 180 to 

1,954 mg/kg) when administered orally. 

In subacute studies (4 weeks) conducted 

by Lee et al. (1978), dogs, rats, and mice 

were fed 2,4-DNT and studied for toxic 

effects. A NOAEL of 5 mg/kg/day was 

established; decreased body weight gain 

and food consumption, neurotoxic 

signs, and lesions in the brain, kidneys, 

and testes occurred at 25 mg/kg/day (the 

highest dose tested). 

Subchronic studies in mice, rats, and 

dogs that administered 2,4- and 2,6-DNT 

in the diet produced similar effects in 

all species. All species exposed to 2,4- 

DNT exhibited methemoglobinemia, 

anemia, bile duct hyperplasia 

sometimes accompanied by hepatic 

degeneration, and depressed 

spermatogenesis. Neurotoxicity and 

renal degeneration occurred in dogs at 

a dose level of 20 mg/kg/day of 2,6-DNT 

(Lee et al., 1976). At a dose level of 25 

mg/kg/day of 2,4-DNT, male and female 

dogs developed impaired muscle 

movement and paralysis, 

methemoglobinemia, aspermatogenesis, 

hemosiderosis of the spleen and liver, 

cloudy swelling of the kidneys, and 

lesions of the brain (Ellis et al., 1985). 


rmajette on DSK29S0YB1PROD with MISCELLANEOUS
Federal Register / Vol. 72, No. 83 / Tuesday, May 1, 2007 / Proposed Rules 24033 

These doses were determined to be 

LOAELs for these studies. 

2,4-DNT has been shown to cause 

reproductive effects in rats, mice, and 

dogs (Ellis et al., 1979; Lee et al., 1985; 

Hong et al., 1985; Ellis et al., 1985). Ellis 

et al. (1979) observed effects in rats 

following dietary exposure after a dose 

of 35 mg/kg/day but not 5 mg/kg/day 

over 3 generations. Male mice fed 2,4- 

DNT for 13 weeks exhibited testicular 

degeneration and atrophy and decreased 

spermatogenesis at 95 mg/kg/day (Hong 

et al., 1985). In another reproductive 

study, dogs exhibited mild to severe 

testicular degeneration and reduced 

spermatogenesis (Ellis et al., 1985) 

when administered 2,4-DNT in capsules 

at 25 mg/kg/day. There are currently no 

studies of the reproductive or 

developmental toxicity of 2,6-DNT 

although a subchronic study in dogs 

identified atrophy of spermatogenic 

cells in males suggesting a one- or twogeneration study as a data need for 2,6- 

DNT. 

Some studies evaluated the effects of 

DNT in the form of a technical mixture 

(tg-DNT). In a study by Price et al. 

(1985), the teratogenic potential of tgDNT (containing approximately 76 

percent 2,4-DNT and 19 percent 2,6- 

DNT) was investigated in rats. The 

study was conducted in two phases to 

evaluate the possible teratogenicity of 

DNT as well as DNT effects on postnatal 

development. For the first phase, rats 

were administered 0, 14, 35, 37.5, 75, 

100, or 150 mg/kg/day of DNT in corn 

oil by gavage. In the postnatal phase, 

rats were administered 14, 35, 37.5, 75, 

or 100 mg/kg/day of DNT in corn oil by 

gavage. The NOAEL and LOAEL for 

developmental toxicity were 14 and 35 

mg/kg/day, respectively, based on 

significant increases in relative liver and 

spleen weight in the fetuses of dams 

administered DNT at levels of 35 mg/kg/ 

day or greater. No teratogenic toxicity 

was seen in the study rats. 

In chronic exposures, oral dietary 

administration of 2,4-DNT to dogs 

primarily affected the nervous system, 

erythrocytes, and biliary tract (Ellis et 

al., 1979, 1985). Based on neurotoxicity, 

hematologic changes, and effects on the 

bile ducts in dogs, the LOAEL was 

determined to be 1.5 mg/kg/day and the 

NOAEL was 0.2 mg/kg/day. EPA 

established an RfD of 0.002 mg/kg/day 

for 2,4-DNT (USEPA, 1992c) based on 

this study. An uncertainty factor of 100, 

to account for interspecies and 

intraspecies variability, was applied to 

derive the RfD. 

EPA established an RfD of 0.001 mg/ 

kg/day for 2,6-DNT (USEPA, 1992c). 

This RfD was also based on 

neurotoxicity, Heinz body formation, 

biliary tract hyperplasia, liver and 

kidney histopathology, and death in 

beagle dogs that were fed gelatin 

capsules containing 2,6-DNT daily for 

up to 13 weeks (Lee et al., 1976). The 

NOAEL for this study was 4 mg/kg/day, 

and an uncertainty factor of 3,000 (100 

for inter- and intra-species variability, 

10 for the use of a subchronic study, 3 

to account for the limited database) was 

applied to derive the RfD. 

DNT is likely to be carcinogenic to 

humans (classified as a B2 carcinogen; 

USEPA, 1990c). This is based on 

significant increases in hepatocellular 

carcinoma and mammary gland tumors 

in female rats fed DNT (98 percent 2,4- 

DNT with 2 percent 2,6-DNT) in the diet 

in a two-year study (Ellis et al., 1979). 

The tumor incidence in the female rats 

was used to establish a slope factor of 

6.67 x 10-1 according to the 1999 EPA 

guidelines. Concentrations of 5 [mu]g/L, 

0.5 [mu]g/L, and 0.05 [mu]g/L are 

associated with carcinogenic risks of 

10-4, 10-5, and 10-6 respectively. There 

were no studies found in the literature 

that evaluated the effects of 2,4- or 2,6- 

DNT on children. There is evidence that 

the pups and fetuses from dams 

administered tg-DNT had significant 

increases in relative liver and spleen 

weights (Price et al., 1985). DNT toxicity 

may be different in children, compared 

to adults, since it undergoes 

bioactivation in the liver and by the 

intestinal microflora (ATSDR, 1998). 

Newborns may be more sensitive to 

DNT-related methemoglobinemia 

because an enzyme that protects against 

increased levels of methemoglobin is 

inactive for a short duration 

immediately after birth (Gruener 1976; 

ATSDR, 1998). However, there are no 

experimental data on differences in 

children’s responses to 2,4-/2,6-DNT. 

c. Occurrence. EPA included both 2,4- 

and 2,6-DNT as analytes in the UCMR 

1. Because the HRL for both 2,4- and 

2,6-DNT (0.05 [mu]g/L) is lower than 

the minimum reporting limit used for 

monitoring (MRL of 2 [mu]g/L), EPA 

used the MRL to evaluate occurrence 

and exposure. The MRL is within the 

10-4 to the 10-6 cancer risk range for 

either 2,4- or 2,6-DNT. In evaluating the 

UCMR 1 data, EPA found that 1 of the 

3,866 PWSs sampled (or 0.03 percent) 

detected 2,4-DNT at the MRL of 2 

[mu]g/L, affecting 0.02 percent of the 

population served (or 38,000 people 

from 226 million). None of the 3,866 

PWSs sampled (serving 226 million) 

detected 2,6-DNT at the MRL of 2 

[mu]g/L (USEPA, 2006a and 2006b). 

EPA also evaluated the results of a 

USGS review of 3 highway and urban 

runoff studies (Lopes and Dionne, 

1998). These studies showed no detects 

for either 2,4- or 2,6-DNT using a 

reporting limit of 5 [mu]g/L (a value 

within the 10-4 to 10-6 risk range). 

d. Preliminary Determination. The 

Agency has made a preliminary 

determination not to regulate 2,4- or 2,6- 

DNT with an NPDWR. Because 2,4- and 

2,6-DNT appear to occur infrequently at 

levels of concern in PWSs, the Agency 

believes that a national primary 

drinking water regulation does not 

present a meaningful opportunity for 

health risk reduction. 2,4-DNT was 

detected only once at a minimum 

reporting level that is within the 10-4 to 

the 10-6 cancer risk range, while 2,6- 

DNT was not detected at this same level 

in any of the PWSs monitored under the 

UCMR 1. 

EPA recognizes that 2,4- and 2,6-DNT 

are listed as probable human 

carcinogens. For this reason, the Agency 

encourages those States with public 

water systems that may have either 2,4- 

or 2,6-DNT above the HRL to evaluate 

site-specific protective measures and to 

consider whether State-level guidance 

(or some other type of action) is 

appropriate. The Agency’s original 

Health Advisories for 2,4- and 2,6-DNT 

were developed for military 

installations. Because the Agency 

recognizes that 2,4- and 2,6-DNT may 

still be found at some military sites, the 

Agency has updated the Health 

Advisories to reflect recent health 

effects publications. The Health 

Advisories are available for review in 

the docket. The updated Health 

Advisories will provide information to 

any States with public water systems 

that may have either 2,4- or 2,6-DNT 

above the HRL. 

8. s-Ethyl dipropylthiocarbamate (EPTC) 

a. Background. EPTC, a synthetic 

organic compound, is a thiocarbamate 

herbicide used to control weed growth 

during the pre-emergence and early 

post-emergence stages of weed 

germination. First registered for use in 

1958, EPTC is used across the U.S. in 

the agricultural production of a number 

of crops, most notably corn, potatoes, 

dried beans, alfalfa, and snap beans. 

EPTC is also used residentially on shade 

trees, annual and perennial 

ornamentals, and evergreens (USEPA, 

1999c). 

Estimates of EPTC usage in the United 

States suggest a decline from 

approximately 17 to 21 million pounds 

active ingredient in 1987 to 

approximately 7 to 9 million pounds 

active ingredient in 1999. TRI data from 

1995 to 2003 indicate that most on-site 

industrial releases of EPTC tend to be 

releases to air and underground 

injections. Surface water discharges are 


rmajette on DSK29S0YB1PROD with MISCELLANEOUS
24034 Federal Register / Vol. 72, No. 83 / Tuesday, May 1, 2007 / Proposed Rules 

minimal in comparison (USEPA, 2006g). 

Total releases for 2003 were 2,183 lbs. 

Environmental fate data indicate that 

EPTC would not be persistent under 

most environmental conditions. 

Volatilization into the atmosphere and 

degradation by soil organisms appear to 

be the primary dissipation routes. EPTC 

has a low affinity for binding to the soil 

so the potential to leach to ground water 

does exist. If EPTC reaches ground 

water, volatilization is less likely to 

occur (USEPA, 1999c). 

b. Health Effects. In acute animal 

toxicity studies, EPTC was shown to be 

moderately toxic via oral and dermal 

routes and highly toxic via inhalation 

exposures. EPTC is a reversible 

cholinesterase (ChE) inhibitor. Similar 

to other thiocarbamates, it does not 

produce a consistent ChE inhibition 

profile. There was no consistent pattern 

observed in any of the toxicity studies 

with regard to species, duration of 

treatment, or the type of ChE enzyme 

measured. Typically, studies showed 

inhibition of plasma ChE with doserelated decreases in red blood cell and 

brain ChE activity. Some studies have 

shown that brain ChE activity was 

inhibited without any effect on either 

plasma or erythrocyte ChE activities. 

Other studies illustrated erythrocyte 

ChE inhibition with no effect on either 

plasma or brain ChE (USEPA, 1999c). In 

a primary eye irritation study in rabbits, 

technical grade EPTC was shown to be 

slightly irritating (USEPA, 1999c). 

In subchronic and chronic studies 

performed in both rats and dogs, there 

was a dose-related increase in the 

incidence and severity of 

cardiomyopathy, a disorder of the heart 

muscle (Mackenzie, 1986; USEPA, 

1999c). An increase in the incidence 

and severity of degenerative effects 

(neuronal and/or necrotic degeneration) 

in both the central and peripheral 

nervous system was observed in rats 

and dogs following exposure to EPTC 

(USEPA, 1999c). 

EPA derived an RfD of 0.025 mg/kg/ 

day for EPTC (USEPA, 1990d; USEPA, 

1999c). This value was calculated using 

a NOAEL of 2.5 mg/kg/day from a study 

by Mackenzie (1986). An uncertainty 

factor of 100 was applied for inter- and 

intraspecies differences. The critical 

effect associated with the RfD is 

cardiomyopathy (disease of the heart 

muscle). In the reregistration of EPTC, 

the application of a ten-fold Food 

Quality Protection Act (FQPA) factor 

was recommended in order to be 

protective against residential exposures 

of infants and children. The Agency 

derived the HRL for EPTC using the RfD 

of 0.025 mg/kg/day and a 20 percent 

relative source contribution. The HRL is 

calculated to be 0.175 mg/L or 175 

[mu]g/L. The Agency used long-term studies in 

mice and rats and short-term studies of 

mutagenicity to evaluate the potential 

for carcinogenicity (USEPA, 1990d). 

Based on these data and using EPA’s 

1999 Guidelines for Carcinogen Risk 

Assessment, EPTC is not likely to be 

carcinogenic to humans (USEPA, 

1999a). 

EPA also evaluated whether health 

information is available regarding the 

potential effects on children and other 

sensitive populations. Data do not 

suggest increased pre- or post-natal 

sensitivity of children and infants to 

EPTC exposure. In animal studies, 

adverse developmental effects (i.e., 

decreased fetal body weight and 

decreased litter size) were only seen at 

doses that were toxic to the mother 

(USEPA, 1999c). Results from both 

developmental and reproductive studies 

indicate that there are only minimal 

adverse effects. The behavior patterns of 

children that lead to heightened 

opportunities for exposure in the indoor 

environment and the need for a 

developmental neurotoxicity study lead 

OPP to recommend the application of a 

ten-fold FQPA factor for EPTC. 

However, EPA did not apply this factor 

in the screening analysis because it does 

not apply to programs other than the 

pesticide registrations. c. Occurrence. EPA included EPTC as 

an analyte in the UCMR 1. None of the 

3,866 PWSs sampled (serving a 

population of 226 million) had detects 

of EPTC at the MRL of 1 [mu]g/L. 

Hence, these data indicate that no 

occurrence and exposure is expected at 

levels greater than 87.5 [mu]g/L (1⁄2 the 

HRL) and greater than 175 [mu]g/L (the 

HRL) (USEPA, 2006a and 2006b). 

EPA also evaluated several sources of 

supplemental information, which 

included: 

<bullet≤ The National Pesticide 

Survey, <bullet≤ The Pesticides in Ground 

Water Database, and 

<bullet≤ The provisional pesticide 

results from the 1992–2001 USGS 

NAWQA survey of ambient surface and 

ground waters across the U.S. As part of the National Pesticide 

Survey, EPA collected samples from 

approximately 1,300 community water 

systems and rural drinking water wells 

between 1988 and 1990. The NPS 

included EPTC as an analyte in the 

monitoring survey. EPTC was not 

detected using a minimum reporting 

limit of 0.15 [mu]g/L (USEPA, 1990a). The Pesticides in Ground Water 

Database (USEPA, 1992b) indicates that 

EPTC was found in 2 of 1,752 ground 

water wells that were sampled in 10 

States. Both contaminated wells were in 

Minnesota. The detected concentrations 

ranged from 0.01 to 0.33 [mu]g/L. All of 

these positive detections are less than 

the HRL of 175 [mu]g/L, as well as 87.5 

[mu]g/L (1⁄2 the HRL). 

The USGS NAWQA program included 

EPTC as an analyte in its 1992–2001 

monitoring survey of ambient surface 

and ground waters across the United 

States. EPA evaluated the results of the 

provisional data, which are available on 

the Web (Martin et al., 2003; Kolpin and 

Martin, 2003). While the USGS detected 

EPTC in both surface and ground 

waters, 95 percent of the samples from 

the various land use settings were less 

than or equal to 0.018 [mu]g/L. The 

estimated maximum surface water 

concentration, 29.6 [mu]g/L (mixed land 

use settings), and the maximum ground 

water concentration, 0.45 [mu]g/L 

(agricultural settings), are both less than 

175 [mu]g/L (the EPTC HRL). 

d. Preliminary Determination. The 

Agency has made a preliminary 

determination not to regulate EPTC with 

an NPDWR. Because EPTC does not 

appear to occur at health levels of 

concern in PWSs, the Agency believes 

that a national primary drinking water 

regulation does not present a 

meaningful opportunity for health risk 

reduction. While EPTC has been found 

in ambient waters, it was detected only 

at levels less than the HRL (as well as 

1⁄2 the HRL) and it was not found in the 

UCMR 1 survey of public water 

supplies. 

9. Fonofos 

a. Background. Fonofos, an 

organophosphate, is a soil insecticide 

used to control pests such as corn 

rootworms, cutworms, symphylans (i.e., 

garden centipedes), and wireworms. 

Primarily used on corn crops, fonofos 

was also used on other crops such as 

asparagus, beans, beets, corn, onions, 

peppers, tomatoes, cole crops, sweet 

potatoes, peanuts, peas, peppermint, 

plantains, sorghum, soybeans, 

spearmint, strawberries, sugarcane, 

sugar beets, white (Irish) potatoes, and 

tobacco (USEPA, 1999d). 

Fonofos was scheduled for a 

reregistration decision in 1999. 

However, before the review was 

completed, the registrant requested 

voluntary cancellation. The cancellation 

was announced in the Federal Register 

on May 6, 1998 (63 FR 25033 (USEPA, 

1998d)), with an effective date of 

November 2, 1998, plus a one-year grace 

period to permit the exhaustion of 

existing stocks (USEPA, 1999d). 

NCFAP data indicate that fonofos use 

declined significantly during the 1990s 

(NCFAP, 2004). According to NCFAP, 


rmajette on DSK29S0YB1PROD with MISCELLANEOUS
Federal Register / Vol. 72, No. 83 / Tuesday, May 1, 2007 / Proposed Rules 24035 

approximately 3.2 million pounds of 

fonofos a.i. were applied annually 

around 1992 and approximately 0.4 

million pounds a.i. were applied 

annually around 1997. The U.S. 

Geological Survey (USGS) estimates an 

average of 2.7 million pounds a.i. were 

used annually around 1992 (Thelin and 

Gianessi, 2000). 

Fonofos is moderately persistent in 

soil and its persistence depends on soil 

type, organic matter, rainfall, and 

sunlight. Since fonofos adsorbs 

moderately well to soil, it is not readily 

leached or transported to ground water 

but it can be transported to surface 

waters in runoff. Fonofos is rapidly 

degraded by soil microorganisms 

(Extoxnet, 1993). Fonofos tends to 

volatilize from wet soil and water 

surfaces, but the process is slowed by 

adsorption to organic material in soil, 

suspended solids, and sediment (HSDB, 

2004d). 

b. Health Effects. Fonofos (like many 

organophosphates) is toxic to humans 

and animals. Case reports and acute oral 

toxicity studies in animals indicate that 

oral exposure to fonofos induces clinical 

signs of toxicity that are typical of 

cholinesterase inhibitors. In humans, 

accidental exposures produced 

symptoms of acute intoxication, nausea, 

vomiting, salivation, sweating, muscle 

twitches, decreased blood pressure and 

pulse rate, pinpoint pupils, profuse 

salivary and bronchial secretions, 

cardiorespiratory arrest, and even death 

in 1 exposed individual (Hayes, 1982; 

Pena Gonzalez et al., 1996). 

In animals, clinical signs of exposure 

included tremors, salivation, diarrhea, 

and labored breathing (USEPA, 1996c). 

Chronic exposure studies also indicated 

that oral administration of fonofos 

inhibits cholinesterase (Banerjee et al., 

1968; Cockrell et al., 1966; Hodge, 1995; 

Horner, 1993; Miller, 1987; Miller et al., 

1979; Pavkov and Taylor, 1988; 

Woodard et al., 1969). Cholinesterase 

inhibition is one of the critical effects 

associated with the RfD, which was 

verified by EPA (USEPA, 1991) at 0.002 

mg/kg/day. EPA derived the RfD of 

0.002 mg/kg/day using a NOAEL of 0.2 

mg/kg/day (Hodge, 1995) and a 100-fold 

uncertainty factor to account for interand intraspecies differences. Fonofos is classified as an unlikely 

human carcinogen (Group E) because 

there is no evidence of carcinogenic 

potential in the available long-term 

feeding studies in rats and mice 

(Banerjee et al., 1968; Pavkov and 

Taylor, 1988; Sprague and Zwicker, 

1987). In addition, fonofos does not 

appear to be mutagenic (USEPA, 1996c). EPA evaluated whether health 

information is available regarding the 

potential effects on children and other 

sensitive populations. In the available 

developmental studies with rabbits 

(Sauerhoff, 1987) and mice (Minor et al., 

1982; Pulsford, 1991), no developmental 

effects were observed at oral doses as 

high as 1.5 mg/kg/day in the rabbit 

(highest dose tested) nor in mice at 

doses as high as 2.0 mg/kg/day (Minor 

et al., 1982; Pulsford, 1991). However, 

in mice, effects were noted at higher 

dose levels. These effects included an 

increase in the incidence of variant 

sternebrae ossifications (at 6 mg/kg/day 

or greater) and a slight dilation of the 

fourth brain ventricle in offspring (at 4 

mg/kg/day or greater). No 

developmental neurotoxicity study with 

fonofos is available for further 

assessment of this endpoint. In a threegeneration reproduction study in rats 

(Woodard et al., 1968), no treatmentrelated adverse effects were observed at 

the 2 dose levels used in this study, 0.5 

and 1.58 mg/kg/day. The Agency believes that the current 

RfD is adequately protective of children. 

The current fonofos RfD of 0.002 mg/kg/ 

day is 1000-fold lower than the NOAEL 

observed in the Woodard et al. (1968) 

developmental studies. Using the RfD of 0.002 mg/kg/day for 

fonofos and a 20 percent screening 

relative source contribution, the Agency 

derived an HRL of 0.014 mg/L and 

rounded to 0.01 mg/L (or 10 [mu]g/L). c. Occurrence. EPA included fonofos 

as an analyte in the UCMR 1 List 2 

Screening Survey. None of the 2,306 

samples from the 295 PWSs sampled 

(serving a population of 41 million) 

contained detects for fonofos at the MRL 

of 0.5 [mu]g/L. Hence, these data 

indicate that no occurrence and 

exposure is expected at levels greater 

than 5 [mu]g/L (1⁄2 the HRL) and greater 

than 10 [mu]g/L (the HRL) (USEPA, 

2006a and 2006b). 

The USGS NAWQA program included 

fonofos as an analyte in its 1992–2001 

monitoring survey of ambient surface 

and ground waters across the United 

States. EPA evaluated the results of the 

provisional data, which are available on 

the Web (Martin et al., 2003; Kolpin and 

Martin, 2003). While the USGS detected 

fonofos in both surface and ground 

waters, 95 percent of the samples from 

the various land use settings were less 

than 0.003 [mu]g/L (the reporting limit). 

The maximum surface water 

concentration, 1.20 [mu]g/L 

(agricultural setting), and the maximum 

ground water concentration, 0.009 

[mu]g/L (agricultural setting), are both 

less than 10 [mu]g/L and less than 5 

[mu]g/L (the fonofos HRL and 1⁄2 the 

HRL). 

d. Preliminary Determination. The 

Agency has made a preliminary 

determination not to regulate fonofos 

with an NPDWR. Because fonofos does 

not appear to occur at health levels of 

concern in PWSs, the Agency believes 

that a national primary drinking water 

regulation does not present a 

meaningful opportunity for health risk 

reduction. While fonofos has been 

found in ambient waters, it was detected 

only at levels less than the HRL (as well 

as 1⁄2 the HRL) and it was not found in 

UCMR 1 Screening Survey of public 

water supplies. Fonofos was voluntarily 

cancelled in 1998 and the Agency 

expects any remaining stocks and 

releases into the environment to 

decline. In addition, since fonofos tends 

to bind strongly to soil, any releases to 

the environment are not likely to 

contaminant source waters. 

10. Terbacil 

a. Background. Terbacil, a synthetic 

organic compound, is a selective 

herbicide used to control broadleaf 

weeds and grasses on terrestrial food/ 

feed crops (e.g., apples, mint, 

peppermint, spearmint, and sugarcane), 

terrestrial food (e.g., asparagus, 

blackberry, boysenberry, dewberry, 

loganberry, peach, raspberry, 

youngberry, and strawberry), terrestrial 

feed (e.g., alfalfa, forage, and hay) and 

forest trees (e.g., cottonwood) (USEPA, 

1998e). 

In 1998, EPA estimated that 

agricultural usage of terbacil consumed 

approximately 221,000 to 447,000 

pounds of active ingredient annually 

and non-agricultural usage consumed 

approximately 9,000 to 14,000 pounds. 

These estimates are based on data 

collected mostly between 1990 and 

1995, and in some cases as early as 1987 

(USEPA, 1998e). According to NCFAP 

(2004), approximately 298,000 pounds 

of terbacil a.i. were applied annually in 

agriculture around 1992 and 

approximately 342,000 pounds a.i. were 

applied around 1997. 

Terbacil is listed as a TRI chemical 

and data are reported from one or more 

facilities in a single state, Texas, for the 

time period covering 1995 to 1997. 

During this three-year period, all 

reported releases were on-site releases 

to surface water that varied between 

3,000 to 10,000 pounds annually 

(USEPA, 2006h). 

Terbacil is considered a persistent 

and potentially mobile herbicide in 

terrestrial environments. Because of its 

low affinity to soils, it can potentially 

leach into ground and/or surface waters 

(USEPA, 1998e; Extoxnet, 1994). 

b. Health Effects. In acute and 

subchronic toxicity studies, terbacil is 

practically non-toxic (Haskell 

Laboratories, 1965a and 1965b). Terbacil 

does not cause dermal sensitivity in 


rmajette on DSK29S0YB1PROD with MISCELLANEOUS
24036 Federal Register / Vol. 72, No. 83 / Tuesday, May 1, 2007 / Proposed Rules 

rabbits or guinea pigs and causes mild 

conjunctival eye irritation in rabbits 

(Henry, 1986; Hood, 1966). In rats 

exposed subchronically to dietary 

terbacil, effects were seen at a LOAEL of 

25 mg/kg/day and included increased 

absolute and relative liver weights, 

vacuolization, and enlargement of liver 

cells (Wazeter et al.,1964; Haskell 

Laboratories, 1965c). 

A primary target organ in rats 

following exposure to terbacil is the 

liver. Chronic effects of dietary terbacil 

exposure in two-year studies included 

increases in thyroid-to-body weight 

ratios, slight increases in liver weights 

and elevated alkaline phosphatase 

levels in beagle dogs, significant 

decreases in body weight in rats, 

increases in serum cholesterol levels 

and increases in liver to body weight 

ratios in rats (Wazeter et al.,1967a; 

Malek, 1993). In beagle dogs, effects 

were seen at or above 6.25 mg/kg/day 

(NOAEL = 1.25 mg/kg/day). In rats, 

effects (i.e., decreases in body weight, 

increases in liver weights and 

cholesterol levels) were seen at higher 

levels (LOAELs = 56 mg/kg/day for 

males and 83 mg/kg/day for females). Terbacil is not considered to be a 

developmental or reproductive toxicant. 

In developmental studies, maternal 

effects were generally seen prior to or at 

the same levels as developmental 

effects. Haskell Laboratories (1980) 

reported maternal effects (i.e., decreased 

body weight) and significant decreases 

in the number of live fetuses per litter 

due to early fetal resorption at a LOAEL 

of 62.5 mg/kg/day in rats. In rabbits 

administered terbacil via gavage, the 

maternal and developmental LOAELs 

were equal (600 mg/kg/day). Maternal 

toxicity was based on the death of the 

dams and developmental toxicity was 

based on a decrease in live fetal weights 

(Solomon, 1984). No reproductive 

effects were seen in a three-generation 

study where terbacil was administered 

to male and female rats at dose levels of 

2.5 and 12.5 mg/kg/day (Wazeter et al., 

1967b). 

Terbacil is not mutagenic. Terbacil 

was tested and found negative in a 

chromosomal aberration study in rat 

bone marrow cells, found negative in a 

gene mutation assay (with and without 

S9 activation), and found negative for 

DNA synthesis when tested up to 

cytotoxic levels in rats (Cortina, 1984; 

Haskell Laboratories,1984). Terbacil 

shows no evidence of carcinogenicity 

and is unlikely to be carcinogenic to 

humans (Group E) (USEPA, 1998e). The RfD of 0.013 mg/kg/day for 

terbacil (USEPA, 1998e) is calculated 

from a two-year chronic study in beagle 

dogs. The LOAEL of 6.25 mg/kg/day 

was based on increased thyroid-to-body 

weight ratios, slight increases in liver 

weights, and elevated alkaline 

phosphatase levels with a NOAEL of 

1.25 mg/kg/day. In deriving the RfD, the 

Agency applied an uncertainty factor of 

100 to account for interspecies and 

intraspecies differences. Using the RfD 

of 0.013 mg/kg/day and applying a 20 

percent screening relative source 

contribution, the Agency derived an 

HRL of 0.090 mg/L (or 90 g/L) for 

terbacil. 

EPA also evaluated whether health 

information is available regarding the 

potential effects on children and other 

sensitive populations. In the case of 

terbacil, the Agency determined that 

there was no need to apply an FQPA 

factor to the RfD in order to protect 

children (USEPA, 1998e). Other 

potentially sensitive subpopulations 

have not been identified. c. Occurrence. EPA included terbacil 

as an analyte in UCMR 1. None of the 

3,866 PWSs sampled (serving a 

population of 226 million) had detects 

for terbacil at the MRL of 2 g/L. Hence, 

these data indicate that no occurrence 

and exposure is expected at levels 

greater than 45 g/L (1⁄2 the HRL) and 

greater than 90 [mu]g/L (the terbacil 

HRL) (USEPA, 2006a and 2006b). 

EPA also evaluated several sources of 

supplemental information, which 

included: 

<bullet≤ The National Pesticide 

Survey, <bullet≤ The Pesticides in Ground 

Water Database, and 

<bullet≤ The provisional pesticide 

results from the 1992–2001 USGS 

NAWQA survey of ambient surface and 

ground waters across the U.S. As part of the National Pesticide 

Survey, EPA collected samples from 

approximately 1,300 community water 

systems and rural drinking water wells 

between 1988 and 1990. The NPS 

included terbacil as an analyte in the 

monitoring survey. Terbacil was not 

detected using a minimum reporting 

limit of 1.7 [mu]g/L (USEPA, 1990a). The Pesticides in Ground Water 

Database (USEPA, 1992b) indicates that 

terbacil was found in 6 of the 288 

ground water wells tested for this 

contaminant in 6 States. Terbacil was 

found in 1 ground water well in Oregon 

(at a concentration of 8.9 [mu]g/L) and 

5 ground water wells in West Virginia 

(with concentrations ranging from 0.3 to 

1.2 [mu]g/L). All of the positive 

detections are less than the HRL of 90 

[mu]g/L, as well as 45 [mu]g/L (1⁄2 the 

HRL). 

The USGS NAWQA program included 

terbacil as an analyte in its 1992–2001 

monitoring survey of ambient surface 

and ground waters across the United 

States. EPA evaluated the results of the 

provisional data, which are available on 

the Web (Martin et al., 2003; Kolpin and 

Martin, 2003). While the USGS detected 

terbacil in both surface and ground 

waters, 95 percent of the samples from 

the various land use settings were less 

than 0.034 [mu]g/L (the USGS reporting 

limit). The maximum surface water 

concentration, 0.54 [mu]g/L 

(agricultural setting), and the maximum 

ground water concentration, 0.891 

[mu]g/L (mixed land use setting), are 

both less than 90 [mu]g/L and less than 

45 [mu]g/L (the terbacil HRL and 1⁄2 the 

HRL). 

d. Preliminary Determination. The 

Agency has made a preliminary 

determination not to regulate terbacil 

with an NPDWR. Because terbacil does 

not appear to occur at health levels of 

concern in PWSs, the Agency believes 

that a national primary drinking water 

regulation does not present a 

meaningful opportunity for health risk 

reduction. Terbacil has been found in 

ambient waters but the levels were less 

than the HRL (as well as 1⁄2 the HRL). 

It was not found in the UCMR 1 survey 

of public water supplies. 

11. 1,1,2,2-Tetrachloroethane 

a. Background. 1,1,2,2- 

Tetrachloroethane, a volatile organic 

compound, is not known to occur 

naturally in the environment (IARC, 

1979). Prior to the 1980s, 1,1,2,2- 

tetrachloroethane was synthesized for 

use in the production of other 

chemicals, primarily chlorinated 

ethylenes. 1,1,2,2-Tetrachloroethane 

was also once used as a solvent to clean 

and degrease metals, in paint removers, 

varnishes, lacquers, and photographic 

films, and for oil/fat extraction (Hawley, 

1981). Commercial production of 

1,1,2,2-tetrachloroethane in the U.S. 

ceased in the 1980s when other 

processes to generate chlorinated 

ethylenes were discovered (ATSDR, 

1996). 

Production of 1,1,2,2- 

tetrachloroethane in the U.S. was 

approximately 440 million pounds in 

1967 (Konietzko, 1984). Production 

declined to an estimated 34 million 

pounds by 1974 (ATSDR, 1996). 

Although U.S. commercial production 

ceased in the 1980s, 1,1,2,2- 

tetrachloroethane is still generated as a 

byproduct and/or intermediate in the 

production of other chemicals. TRI data 

indicate that environmental releases 

have generally declined from a high of 

about 175,000 pounds in 1988 to a low 

of 3,500 pounds in 2003. Most releases 

took the form of air emissions, though 

surface water discharges were also 

documented nearly every year (USEPA, 

2006i). 


rmajette on DSK29S0YB1PROD with MISCELLANEOUS
Federal Register / Vol. 72, No. 83 / Tuesday, May 1, 2007 / Proposed Rules 24037 

Volatilization from water or soil 

surfaces to the atmosphere appears to be 

the primary dissipation route for 1,1,2,2- 

tetrachloroethane. In subsurface soils 

and ground water, 1,1,2,2- 

tetrachloroethane is subject to 

biodegradation by soil organisms and/or 

chemical hydrolysis by water (ATSDR, 

1996). 

b. Health Effects. Data on the toxicity 

of 1,1,2,2-tetrachloroethane in humans 

are limited, consisting of one 

experimental inhalation study, a few 

case reports of suicidal or accidental 

ingestion, and dated occupational 

studies. In most cases, there was no 

quantification of the exposure. 

Respiratory and mucosal effects, eye 

irritation, nausea, vomiting, and 

dizziness were reported by human 

volunteers exposed to 1,1,2,2- 

tetrachloroethane vapors under 

controlled chamber conditions 

(Lehmann and Schmidt-Kehl, 1936). 

Effects from non-lethal occupational 

exposures included gastric distress (i.e., 

pain, nausea, vomiting), headache, loss 

of appetite, an enlarged liver, and 

cirrhosis (Jeney et al., 1957; LoboMendonca, 1963; Minot and Smith, 

1921). 

There have been a variety of animal 

studies in rats and mice using both the 

inhalation and oral exposure routes. 

Recent studies by the National 

Toxicology Program (NTP, 2004) 

provide a detailed evaluation of the 

short-term and subchronic oral toxicity 

of 1,1,2,2-tetrachloroethane and confirm 

many of the observations from earlier 

studies. In rats and mice exposed orally, 

the liver appears to be the primary target 

organ. The RfD (10 [mu]g/kg/day) for 

1,1,2,2-tetrachloroethane was derived 

from the BMDL for a 1 standard 

deviation change in relative liver 

weight, a biomarker for liver toxicity. A 

1,000-fold uncertainty factor was 

applied in the RfD determination. A National Cancer Institute (1978) 

bioassay of 1,1,2,2-tetrachloroethane 

found clear evidence of carcinogenicity 

in male and female B6C3F1 mice based 

on a dose-related statistically significant 

increase in liver tumors. There was 

equivocal evidence for carcinogenicity 

in Osborn Mendel rats because of the 

occurrence of a small number of rarefor-the species neoplastic and 

preneoplastic lesions in the livers of the 

high dose animals. The Agency used the 

slope factor of 8.5 x 10-2 for the tumors 

in female mice to derive the HRL of 0.4 

[mu]g/L for use in the analysis of the 

occurrence data for 1,1,2,2- 

tetrachloroethane. Information on the 

reproductive effects of 1,1,2,2- 

tetrachloroethane is limited. There is a 

single one-generation inhalation study 

that does not follow a standard 

methodology and examined a small 

number of rats (5 females and 7 males) 

exposed via inhalation to 1 dose (13.3 

mg/m3). There were no statistically 

significant differences in the percentage 

of females having offspring, number of 

pups per litter, average birth weight, sex 

ratio, or post natal offspring mortality 

(Schmidt et al., 1972). Effects on sperm 

in male rats were seen after oral (27 mg/ 

kg/day; NTP, 2004) and inhalation (13 

mg/m3; Schmidt et al., 1972) exposures. 

Similar effects were seen in mice but at 

higher doses. Fetal toxicity did not 

occur in the absence of maternal 

toxicity. Developmental range-finding studies 

conducted for NTP (1991a and b) found 

that 1,1,2,2-tetrachloroethane was toxic 

to the dams and pups of Sprague 

Dawley rats and CD–1 Swiss mice. Rats 

were more sensitive than mice. The 

NOAEL in the rats for both maternal 

toxicity and associated fetal toxicity was 

34 mg/kg/day with a LOAEL of 98 mg/ 

kg/day. In mice, the NOAEL was 987 

mg/kg/day and the LOAEL was 2,120 

mg/kg/day. EPA also evaluated whether health 

information is available regarding the 

potential effects on children and other 

sensitive populations. Individuals with 

preexisting liver and kidney damage 

would likely be sensitive to 1,1,2,2- 

tetrachloroethane exposure. Low intake 

of antioxidant nutrients (e.g., Vitamin E, 

Vitamin C, and selenium) could be a 

predisposing factor for liver damage. In 

addition, individuals with a genetically 

low capacity to metabolize 

dichloroacetic acid (the primary 

metabolite of 1,1,2,2-tetrachloroethane) 

may be at greater risk than the general 

population as a result of 1,1,2,2- 

tetrachloroethane exposure. c. Occurrence. EPA included 1,1,2,2- 

tetrachloroethane as an analyte in the 

UCM Round 1 and UCM Round 2 

surveys. EPA evaluated the UCM Round 

1 Cross Section and the UCM Round 2 

Cross Section data at levels greater than 

0.2 [mu]g/L (1⁄2 the HRL) and greater 

than 0.4 [mu]g/L (the HRL) (USEPA, 

2006a and 2006c). The MRLs for UCM 

Round 1 ranged from 0.1 to 10 [mu]g/ 

L and the MRLs for UCM Round 2 

ranged from 0.1 to 2.5 [mu]g/L. Because 

some of the reporting limits exceeded 

the thresholds of interest, the 

occurrence analyses may result in an 

underestimate of systems affected. 

However, all the MRL values used for 

UCM Round 1 and UCM Round 2 are 

within the 10-4 to the 10-6 cancer risk 

range. Analysis of UCM Round 1 Cross 

Section data indicates that 

approximately 0.22 percent (or 44) of 

the 20,407 PWSs sampled had 

detections of 1,1,2,2-tetrachloroethane 

at levels greater than 0.20 [mu]g/L (1⁄2

the HRL), affecting approximately 1.69 

percent of the population served (or 1.6 

million of 95 million). The UCM Round 

1 Cross Section data indicate that 

approximately 0.20 percent (or 41) of 

the 20,407 PWSs sampled had 

detections of 1,1,2,2-tetrachloroethane 

at levels greater than 0.4 [mu]g/L (the 

HRL), affecting approximately 1.63 

percent of the population served (or 1.5 

million of 95 million). The 99th 

percentile of all detects is 112 [mu]g/L 

and the maximum reported value is 200 

[mu]g/L. Analysis of the UCM Round 2 Cross 

Section data indicate that approximately 

0.07 percent (or 18) of the 24,800 PWSs 

sampled had detections of 1,1,2,2- 

tetrachloroethane at levels greater than 

0.2 [mu]g/L (1⁄2 the HRL), affecting 

approximately 0.51 percent of the 

population served (or 362,000 of 71 

million). The UCM Round 2 Cross 

Section data indicate that approximately 

the same percentage and number of the 

PWSs sampled (0.07 percent or 17 of the 

24,800) had detections of 1,1,2,2- 

tetrachloroethane at levels greater than 

0.4 [mu]g/L (the HRL), affecting 

approximately 0.08 percent of the 

population served (or 56,000 of 71 

million). The 99th percentile of all 

detects is 2 [mu]g/L and the maximum 

reported value is 2 [mu]g/L. EPA also evaluated several sources of 

supplemental information, which 

included the USGS VOC National 

Synthesis Random Source Water Survey 

and the Focused Source Water Survey. 

For the Random Source Water Survey, 

the USGS collected samples from 954 

source waters that supply community 

water systems between 1999 and 2000. 

For the Focused Source Water Survey, 

the USGS collected 451 samples from 

134 source waters that supply 

community water systems between 1999 

and 2001. The USGS included 1,1,2,2- 

tetrachloroethane as an analyte in both 

surveys and did not detect it in any of 

the source water samples using a 

reporting limit of 0.2 [mu]g/L (a level 

that is less than the 1,1,2,2- 

tetrachloroethane HRL). In addition, 

USGS did not detect 1,1,2,2- 

tetrachloroethane when using a 

detection level of 0.026 [mu]g/L (a level 

that is over 10 times lower than the 

1,1,2,2-tetrachloroethane HRL) in the 

focused survey (Ivahnenko et al., 2001, 

Grady, 2003, Delzer and Ivahnenko, 

2003a). 

d. Preliminary Determination. The 

Agency has made a preliminary 

determination not to regulate 1,1,2,2- 

tetrachloroethane with an NPDWR. 

Because 1,1,2,2-tetrachloroethane 

appears to occur infrequently at health 

levels of concern in PWSs, the Agency 


rmajette on DSK29S0YB1PROD with MISCELLANEOUS
24038 Federal Register / Vol. 72, No. 83 / Tuesday, May 1, 2007 / Proposed Rules 

18 DWEL = [(Reference Dose x Body Weight of 70 

kg) / Drinking Water Intake of 2 L per day]. 

believes that a national primary 

drinking water regulation does not 

present a meaningful opportunity for 

health risk reduction. While 1,1,2,2- 

tetrachloroethane was detected in both 

the UCM Round 1 and the UCM Round 

2 surveys, the percentage of detections 

had decreased by the time the UCM 

Round 2 survey was performed in the 

mid-1990’s. In addition, the USGS did 

not detect 1,1,2,2-tetrachloroethane in 

two subsequent monitoring surveys of 

source waters that supply community 

water systems using a reporting limit 

that is less than the 1,1,2,2- 

tetrachloroethane HRL. The Agency 

believes that this decrease in detections 

occurred because commercial 

production of 1,1,2,2-tetrachloroethane 

ceased in the mid-1980’s. Hence, the 

Agency does not expect 1,1,2,2- 

tetrachloroethane to occur in many 

public water systems today. 

EPA recognizes that 1,1,2,2- 

tetrachloroethane is listed as a likely 

human carcinogen. For this reason, the 

Agency encourages those States with 

public water systems that may have 

1,1,2,2-tetrachloroethane above the HRL 

to evaluate site-specific protective 

measures and to consider whether Statelevel guidance (or some other type of 

action) is appropriate. The Agency also 

plans to update the Health Advisory 

document for 1,1,2,2-tetrachloroethane 

to provide more recent health 

information. The updated Health 

Advisory will provide information to 

any States with public water systems 

that may have 1,1,2,2-tetrachloroethane 

at levels above the HRL. 

V. What Is the Status of the Agency’s 

Evaluation of Perchlorate? 

At this time, the Agency is not making 

a preliminary determination as to 

whether a national primary drinking 

water regulation is needed for 

perchlorate. However, the Agency has 

placed a high priority on making a 

regulatory determination for perchlorate 

and will publish a preliminary 

determination as soon as possible. EPA 

is not able to make a preliminary 

determination at this time because, in 

order to evaluate perchlorate against the 

three SDWA statutory criteria, the 

Agency believes additional information 

may be needed to more fully 

characterize perchlorate exposure and 

determine whether regulating 

perchlorate in drinking water presents a 

meaningful opportunity for health risk 

reduction. This is particularly true if the 

Agency uses food exposure data to first 

calculate a relative source contribution 

(RSC) and corresponding health 

reference level (HRL) below the 

drinking water equivalent level (DWEL) 

18 in order to determine whether 

regulating perchlorate would present a 

meaningful opportunity for health risk 

reduction. However, the Agency is 

considering several other approaches, 

discussed below, for making this 

statutory determination and is 

requesting public comment on the 

strengths and limitations of these 

approaches. 

The following sections explain why 

EPA is not making a preliminary 

regulatory determination for perchlorate 

at this time, and discusses the 

information the Agency has collected to 

date (that may be relevant to making a 

preliminary regulatory determination), 

the additional information the Agency is 

soliciting in this action, and options for 

additional analyses that the Agency may 

conduct to support a regulatory 

determination. Sections V.A through 

V.D provide a summary of the available 

and relevant information/data that the 

Agency has collected and reviewed 

regarding the sources of perchlorate in 

the environment, its potential health 

effects, and its occurrence in drinking 

water, food, human urine, breast milk, 

and amniotic fluid. Section V.E explains 

the Agency’s basis for not making a 

preliminary regulatory determination 

for perchlorate at this time and Section 

V.F. presents the options the Agency is 

considering to better characterize 

perchlorate exposure and the alternate 

approaches that EPA is considering for 

making a preliminary regulatory 

determination. This action provides an 

opportunity for the public to submit 

other relevant data that may further 

characterize exposure to perchlorate 

through the consumption of foods and/ 

or through other pathways and to 

comment on these alternate approaches. 

The Agency in particular seeks 

comment on the use of urine 

biomonitoring data in estimating 

perchlorate exposure. The Agency will 

consider any relevant information/data 

provided in response to this action as 

the Agency determines whether to 

regulate perchlorate with a national 

primary drinking water regulation and 

how best to proceed to address 

perchlorate. 

A. Sources of Perchlorate 

Perchlorate (ClO4

-

) is an anion 

commonly associated with the solid 

salts of ammonium, magnesium, 

potassium, and sodium perchlorate. 

Perchlorate salts are highly soluble in 

water, and because perchlorate sorbs 

poorly to mineral surfaces and organic 

material, perchlorate can be mobile in 

surface and subsurface aqueous 

environments. Although commonly 

known as a man-made chemical, 

perchlorate also may be derived from 

natural processes. 

While perchlorate has a wide variety 

of industrial uses, it is primarily used in 

the form of ammonium perchlorate as 

an oxidizer in solid fuels used to power 

rockets, missiles, and fireworks. 

Approximately 90 percent of 

perchlorate is manufactured for this 

application (Wang et al., 2002). 

Perchlorate can also be present as an 

ingredient or as an impurity in road 

flares, lubricating oils, matches, 

aluminum refining, rubber 

manufacturing, paint and enamel 

manufacturing, leather tanning, paper 

and pulp processing (as an ingredient in 

bleaching powder), and as a dye 

mordant. 

Perchlorate can also occur naturally 

in the environment. Chile possesses 

caliche ores rich in sodium nitrate 

(NaNO3), which are also a natural 

source of perchlorate (Schilt, 1979 and 

Ericksen, 1983). These Chilean nitrate 

salts (saltpeter) have been mined and 

refined to produce commercial 

fertilizers, which before 2001 accounted 

for about 0.14 percent of U.S. fertilizer 

application (USEPA, 2001d). The 

USEPA (2001d) conducted a broad 

survey of fertilizers and other raw 

materials and found that all products 

surveyed were devoid of perchlorate 

except for those known to contain or to 

be derived from mined Chilean 

saltpeter. 

Perchlorate has also been found in 

other geologic materials. Orris et al. 

(2003) measured perchlorate at levels 

exceeding 1,000 parts per million (ppm 

or mg/kg) in several samples of natural 

minerals, including potash ore from 

New Mexico and Saskatchewan 

(Canada), playa crust from Bolivia, and 

hanksite from California. 

Texas Tech University Water 

Resources Center conducted a largescale sampling program to determine 

the source and distribution of 

perchlorate in northwest Texas 

groundwater (Jackson et al., 2004; 

Rajagopalan et al., 2006). Perchlorate 

was detected at concentrations greater 

than 0.5 g/L in 46 percent of public 

wells and 47 percent of private wells. 

Jackson et al. (2004) hypothesized that 

atmospheric production and/or surface 

oxidative weathering is the source of the 

perchlorate. In related research, 

Dasgupta et al. (2005) detected 

perchlorate in many rain and snow 

samples and demonstrated that 

perchlorate is formed by a variety of 

simulated atmospheric processes 

suggesting that natural, atmosphericallyVerDate Mar 15 2010 08:52 Aug 04, 2010 Jkt 220001 PO 00000 Frm 00024 Fmt 4701 Sfmt 4702 E:\TEMP\01MYP2.LOC 01MYP2

rmajette on DSK29S0YB1PROD with MISCELLANEOUS
Federal Register / Vol. 72, No. 83 / Tuesday, May 1, 2007 / Proposed Rules 24039 

derived perchlorate exists in the 

environment. Barron et al. (2006) 

developed a method for the rapid 

determination of perchlorate in 

rainwater samples, with a detection 

limit between 70 and 80 ng/L. Of the ten 

rainwater samples collected in Ireland 

in 2005, perchlorate was detected in 4 

samples at concentrations between 

0.075 and 0.113 g/L, and in 1 other 

sample at 2.8 g/L. Kang et al. (2006) 

conducted seven-day experiments to 

determine if it was possible to produce 

perchlorate by exposing various 

chlorine intermediates to UV radiation 

in the form of high intensity UV lamps 

and/or ambient solar radiation. 

Perchlorate formation was demonstrated 

in aqueous salt solutions with initial 

concentrations of hypochlorite, chlorite, 

or chlorate between 100 and 10,000 mg/ 

L. 

After a limited investigation, the 

Massachusetts Department of 

Environmental Quality (MA DEP, 2005) 

found that perchlorate may be present 

in sodium hypochlorite solutions used 

in water and wastewater treatment 

plants, and that the level of occurrence 

depends upon storage conditions and 

the initial purity of the stock solution 

(MA DEP, 2005). According to MA DEP 

(2005), the Town of Tewksbury 

conducted a small study to evaluate the 

impact of storage conditions 

(temperature and light) on a new 

shipment of sodium hypochlorite stock 

solution. Tewksbury found that the 

perchlorate concentration in the new 

stock solution increased from 0.2 g/L to 

levels ranging from 995 to 6,750 g/L 

depending on the storage conditions. 

Accounting for the large dilution factor 

(e.g., 20,000 to 1 ratio) used in 

chlorination processes at drinking water 

treatment plants, MA DEP (2005) 

concluded that ‘‘absent additional 

efforts to minimize breakdown of 

hypochlorite solutions, it would appear 

that low levels of the perchlorate ion 

(0.2 to 0.4 g/L) detected in a drinking 

water supply disinfected with sodium 

hypochlorite solutions could be 

attributable to the chlorination process.’’ 

It is not clear at this time what 

proportion of perchlorate found in 

public water supplies or entering the 

food chain comes from these various 

anthropogenic and natural sources. The 

significance of different sources 

probably varies regionally. A study by 

Dasgupta et al. (2006) analyzes the three 

principal sources of perchlorate and 

their relative contributions to the food 

chain. These are its use as an oxidizer 

including rocket propellants, Chilean 

nitrate used principally as fertilizer, and 

that produced by natural atmospheric 

processes. 

B. Health Effects 

Perchlorate can interfere with the 

normal functioning of the thyroid gland 

by competitively inhibiting the 

transport of iodide into the thyroid. 

Iodide is an important component of 

two thyroid hormones, T4 and T3, and 

the transfer of iodide from the blood 

into the thyroid is an essential step in 

the synthesis of these two hormones. 

Iodide transport into the thyroid is 

mediated by a protein molecule known 

as the sodium (Na+)—iodide (I-) 

symporter (NIS). NIS molecules bind 

iodide with very high affinity, but they 

also bind other ions that have a similar 

shape and electric charge, such as 

perchlorate. The binding of these other 

ions to the NIS inhibits iodide transport 

into the thyroid, which can result in 

intrathyroidal iodide deficiency and 

consequently decreased synthesis of T4 

and T3. There is compensation for 

iodide deficiency, however, such that 

the body maintains the serum 

concentrations of thyroid hormones 

within narrow limits through feedback 

control mechanisms. This feedback 

includes increased secretion of thyroid 

stimulating hormone (TSH) from the 

pituitary gland, which has among its 

effects the increased production of T4 

and T3 (USEPA, 2005e). Sustained 

changes in thyroid hormone and TSH 

secretion can result in thyroid 

hypertrophy and hyperplasia (abnormal 

growth or enlargement of the thyroid) 

(USEPA, 2005e). 

In January 2005, the National 

Research Council (NRC) of the National 

Academies of Science (NAS) published 

‘‘Health Implications of Perchlorate 

Ingestion,’’ a review of the current state 

of the science regarding potential 

adverse health effects of perchlorate 

exposure and mode-of-action for 

perchlorate toxicity (NRC, 2005). Based 

on recommendations of the NRC, EPA 

chose data from the Greer et al. (2002) 

human clinical study as the basis for 

deriving a reference dose (RfD) for 

perchlorate (USEPA, 2005e). Greer et al. 

(2002) report the results of a wellcontrolled study that measured thyroid 

iodide uptake, hormone levels, and 

urinary iodide excretion in a group of 24 

healthy adults administered perchlorate 

doses orally over a period of 14 days. 

Dose levels ranged from 0.007 to 0.5 mg/ 

kg/day in the different experimental 

groups. No significant differences were 

seen in measured serum thyroid 

hormone levels (T3, T4, total and free) 

in any dose group. The statistical no 

observed effect level (NOEL) for 

perchlorate-induced inhibition of 

thyroid iodide uptake was 0.007 mg/kg/ 

day. Although the NRC committee 

concluded that hypothyroidism is the 

first adverse effect in the continuum of 

effects of perchlorate exposure, NRC 

recommended that ‘‘the most healthprotective and scientifically valid 

approach’’ was to base the perchlorate 

RfD on the inhibition of iodide uptake 

by the thyroid (NRC, 2005). NRC 

concluded that iodide uptake inhibition, 

although not adverse, is the key 

biochemical event in the continuum of 

possible effects of perchlorate exposure 

and would precede any adverse health 

effects of perchlorate exposure. The 

lowest dose (0.007 mg/kg/day) 

administered in the Greer et al. (2002) 

study was considered a NOEL (rather 

than a NOAEL) because iodide uptake 

inhibition is not an adverse effect but a 

biochemical change (USEPA, 2005e). A 

summary of the data considered and the 

NRC deliberations can be found in the 

NRC report (2005) and the EPA 

Integrated Risk Information System 

(IRIS) summary (USEPA, 2005e). 

The NRC recommended that EPA 

apply an intraspecies uncertainty factor 

of 10 to the NOEL to account for 

differences in sensitivity between the 

healthy adults in the Greer et al. (2002) 

study and the most sensitive 

population, fetuses of pregnant women 

who might have hypothyroidism or 

iodide deficiency. Because the fetus 

depends on an adequate supply of 

maternal thyroid hormone for its central 

nervous system development during the 

first trimester of pregnancy, iodide 

uptake inhibition from low-level 

perchlorate exposure has been 

identified as a concern in connection 

with increasing the risk of 

neurodevelopmental impairment in 

fetuses of high-risk mothers (NRC, 

2005). The NRC (2005) viewed the 

uncertainty factor of 10 as conservative 

and health protective given that the 

point of departure is based on a nonadverse effect (iodide uptake inhibition) 

that precedes the adverse effect in a 

continuum of possible effects of 

perchlorate exposure. NRC concluded 

that no uncertainty factor was needed 

for the use of a less-than chronic study, 

for deficiencies in the database, or for 

interspecies variability. To protect the 

most sensitive human population from 

chronic perchlorate exposure, EPA 

derived an RfD of 0.0007 mg/kg/day 

with a ten-fold total uncertainty factor 

from the NOEL of 0.007 mg/kg/day 

(USEPA, 2005e). 

Blount et al. (2006b) recently 

published a study examining the 

relationship between urinary levels of 

perchlorate and serum levels of TSH 

and total T4 in 2,299 men and women 

(ages 12 years and older), who 

participated in CDC’s 2001–2002 


rmajette on DSK29S0YB1PROD with MISCELLANEOUS
24040 Federal Register / Vol. 72, No. 83 / Tuesday, May 1, 2007 / Proposed Rules 

19 While CDC researchers measured urinary 

perchlorate concentration for 2,820 NHANES 

participants, TSH and total T4 serum levels were 

only available for 2,299 of these participants. 20 WHO notes that the prevalence of goiter begins 

to increase in populations with a median iodide 

intake level below 100 [mu]g/L (WHO, 1994). 

21 EPA Method 314.0 was the analytical method 

approved and used for UCMR 1 at the time of data 

collection. 

22 EPA acknowledges that uncertainties exist in 

the population-served estimates for this alternative 

assessment since the population for a system is 

assumed to be equally distributed across the entry 

points for that system. Because the actual 

population-served by an entry point is not known, 

this alternative approach has an equal chance of 

underestimating or overestimating the actual 

population-served by entry points with positive 

detections for perchlorate. In addition, this 

approach could underestimate the population 

served that is potentially exposed to perchlorate 

and overestimate the level of exposure because it 

can not incorporate the effects of mixing of water 

between different entry points within the 

distribution system. This is because the approach 

cannot account for the dilution that may occur 

when water that has no detections of perchlorate is 

mixed within the distribution system with water 

that has positive detections for perchlorate. 

National Health and Nutrition 

Examination Survey (NHANES).19

Blount et al. (2006b) evaluated 

perchlorate along with covariates 

known or likely to be associated with T4 

or TSH levels to assess the relationship 

between perchlorate and these 

hormones, and the influence of other 

factors on this relationship. These 

covariates included sex, age, race/ 

ethnicity, body mass index, serum 

albumin, serum cotinine (a marker of 

tobacco smoke exposure), estimated 

total caloric intake, pregnancy status, 

post-menopausal status, premenarche 

status, serum C-reactive protein, hours 

fasting before sample collection, urinary 

thiocyanate, urinary nitrate, and use of 

selected medications. The study found 

that perchlorate was a significant 

predictor of thyroid hormones in 

women, but not men. After finding 

evidence of gender differences, the 

researchers focused on further analyzing 

the NHANES data for the 1,111 women 

participants. They divided these 1,111 

women into two categories, higheriodide and lower-iodide, using a cut 

point of 100 [mu]g/L of urinary iodide 

based on the World Health Organization 

(WHO) definition of sufficient iodide 

intake.20 Hypothyroid women were 

excluded from the analysis. According 

to the study authors, about 36 percent 

of women living in the United States 

have urinary iodide levels less than 100 

[mu]g/L (Caldwell et al., 2005). For 

women with urinary iodide levels less 

than 100 [mu]g/L, the study found that 

urinary perchlorate is associated with a 

decrease in (a negative predictor for) T4 

levels and an increase in (a positive 

predictor for) TSH levels. For women 

with urinary iodide levels greater than 

or equal to 100 [mu]g/L, the researchers 

found that perchlorate is a significant 

positive predictor of TSH but not a 

predictor of T4. The study found that 

perchlorate was not a significant 

predictor of T4 or TSH in men. The 

researchers state that perchlorate could 

be a surrogate for another unrecognized 

determinant of thyroid function. Also, 

the study reports that while large doses 

of perchlorate are known to decrease 

thyroid function, this is the first time an 

association of decreased thyroid 

function has been observed at these low 

levels of perchlorate exposure. Of note 

is that the vast majority of the 

participants in this group had urinary 

levels of perchlorate corresponding to 

estimated dose levels that are below the 

RfD of 0.0007 mg/kg/day. The clinical 

significance of the variations in T4/TSH 

levels, which were generally within 

normal limits, has not been determined. 

The researchers noted several 

limitations of the study (e.g., 

assumption that urinary perchlorate 

correlates with perchlorate levels in the 

stroma and tissue and preference for 

measurement of free T4 as opposed to 

total T4) and recommended that these 

findings be confirmed in at least one 

more large study focusing on women 

with low urine iodide levels. It is also 

not known whether the association 

between perchlorate and thyroid 

hormone levels is causal or mediated by 

some other correlate of both, although 

the relationship between urine 

perchlorate and total TSH and T4 levels 

persisted after statistical adjustments for 

some additional covariates known to 

predict thyroid hormone levels (e.g., 

total kilocalorie intake, estrogen use, 

and serum C-reactive protein levels). A 

planned follow-up study will include 

additional measures of thyroid health 

and function (e.g., TPO-antibodies, free 

T4). As EPA proceeds towards a 

regulatory determination for 

perchlorate, the Agency will continue to 

review any new findings/studies on 

perchlorate and their relationship to 

thyroid function as they become 

available. 

C. Occurrence in Water, Food, and 

Humans 

1. Sources of Perchlorate. Section 

V.A. summarizes the potential sources 

of perchlorate in the environment. 2. Studies on Perchlorate Occurrence 

in Public Drinking Water Systems and/ 

or Drinking Water Sources. EPA 

included perchlorate as an analyte in 

the 1999 Unregulated Contaminant 

Monitoring Regulation (UCMR 1) and 

collected drinking water occurrence 

data for perchlorate from 3,858 public 

water systems (PWSs) between 2001 and 

2005. EPA analyzed the available UCMR 

1 data on perchlorate at concentrations 

greater than or equal to 4 [mu]g/L, the 

minimum reporting limit (MRL) for EPA 

Method 314.0.21 The Agency found that 

approximately 4.1 percent (or 160) of 

3,858 PWSs that sampled and reported 

under UCMR 1 had at least 1 analytical 

detection of perchlorate (in at least 1 

entry/sampling point) at levels greater 

than or equal to 4 [mu]g/L. These 160 

systems are located in 26 states and 2 

territories. Of these 160 PWSs, 8 are 

small systems (serving 10,000 or fewer 

people) and 152 are large systems 

(serving more than 10,000 people). 

Approximately 1.9 percent (or 637) of 

the 34,193 samples collected (by these 

3,858 PWSs) had positive detections of 

perchlorate at levels greater than or 

equal to 4 [mu]g/L. The maximum 

reported concentration of perchlorate 

was 420 [mu]g/L, which was found in 

a surface water sample from a PWS in 

Puerto Rico. The average concentration 

of perchlorate for those samples with 

positive detections for perchlorate was 

9.85 [mu]g/L and the median 

concentration was 6.40 [mu]g/L. 

These 160 PWSs (with at least 1 

analytical detection for perchlorate at 

levels greater than or equal to 4 [mu]g/ 

L) serve approximately 7.5 percent (or 

16.8 million) of the 225 million people 

served by the 3,858 PWSs that sampled 

and reported results under UCMR 1. 

The 16.8 million population-served 

value represents the total number of 

people served by the 160 PWSs with at 

least one detect. Not all people served 

by these systems necessarily have 

perchlorate in their drinking water. 

Some of these 160 public water systems 

have multiple entry points to the 

distribution system and not all of the 

entry points sampled had positive 

detections for perchlorate in the UCMR 

1 survey. An alternative approach to the 

system-level assessment of populations 

served is to use an assessment at the 

entry (sampling) point level.22 EPA does 

not have population-served values for 

each entry point at the system level. 

However, an assessment can be 

performed by assuming that each entry 

(or sampling) point at a public water 

system serves an equal proportion of the 

total population-served by the system. 

In other words, for the alternative 

assessment, the population served by 

each system is assumed to be equally 

distributed across all entry (or sampling) 

points at each system. For example, if a 

system serves a million people and has 

5 entry points, it is assumed that each 

entry point serves 200,000 people. 

Using this approach and counting only 


rmajette on DSK29S0YB1PROD with MISCELLANEOUS
Federal Register / Vol. 72, No. 83 / Tuesday, May 1, 2007 / Proposed Rules 24041 

the population served for the entry 

points with positive detections 

(concentrations greater than or equal to 

4 [mu]g/L), the total population served 

by these entry points with perchlorate 

detections is approximately 5 million. 

Section V.E provides the number of 

systems and population-served 

estimates for other thresholds of 

interest. 

The California Department of Health 

Services (CA DHS) began monitoring for 

perchlorate in 1997. In 1999, CA DHS 

began requiring monitoring for 

perchlorate for drinking water sources 

that were identified as vulnerable to 

perchlorate contamination under 

California’s own State monitoring 

program (i.e., Unregulated Chemicals for 

which Monitoring is Required). About 

60 percent (or 7,100) of all drinking 

water sources in California (about 

12,000) were monitored for perchlorate 

under the State monitoring program. 

Between June 2001 and June 2006, CA 

DHS (2006) reports that 284 (about 4%) 

of the approximately 7,100 water 

sources that monitored had at least 2 or 

more positive detections for perchlorate 

at concentrations greater than or equal 

to 4 [mu]g/L (the reporting limit). These 

284 sources supply water for 77 

drinking water systems (CA DHS, 2006) 

and represent active and standby 

sources (and exclude inactive, 

destroyed, and abandoned sources, and 

monitoring and agricultural wells) (CA 

DHS, 2006). 

In 2005, the State of Massachusetts’s 

Department of Environment Protection 

(MA DEP) reported monitoring results 

for 85 percent (379 of 450) of its 

community water systems and 86 

percent (212 of 250) of its non-transient, 

non-community water systems. MA DEP 

found that 9 (1.5%) of the 591 public 

water systems detected perchlorate at 

levels greater than or equal to 1 [mu]g/ 

L (the reporting limit used for a 

modified version of EPA Method 314.0). 

MA DEP found that the occurrence of 

perchlorate for these water systems 

could be traced to the use of blasting 

agents, military munitions, fireworks, 

and, to a lesser degree, sodium 

hypochlorite disinfectant (MA DEP, 

2005). 

3. Studies on Perchlorate Occurrence 

in Foods, Plants, Beverages, and Dietary 

Supplements. The Food and Drug 

Administration (FDA), the United States 

Department of Agriculture (USDA), and 

researchers from academia and industry 

have studied perchlorate in foods. Some 

of these studies are described briefly in 

this section, and also summarized in 

Table 4. EPA has concluded that the 

sampling results described in this 

section and Table 4 are too limited to 

characterize food-borne exposure to 

perchlorate on a national scale. The 

sampling data are limited in the types 

of foods sampled, sample sizes, 

geographic coverage, and/or analytical 

method adequacy and many were 

targeted to foods or areas known or 

likely to have elevated levels of 

perchlorate. Section V.F of this action 

describes the limitations of the food 

sampling data and also describes plans 

for including perchlorate as part of the 

FDA’s Total Diet Study. EPA requests 

that commenters provide the Agency 

with any additional data that may 

further characterize the concentrations 

of perchlorate in foods commercially 

available in the U.S. When providing 

data to the Agency, please describe the 

specific locations where the samples 

were collected, including geographic 

location, type of location (e.g., grocery 

store, farmer’s market, commercial field, 

home garden), and the methodologies 

used to select, collect, prepare, and 

analyze the samples. Please include 

available laboratory data reports as well 

as all relevant quality assurance/quality 

control information. 

BILLING CODE 6560–50–P 


rmajette on DSK29S0YB1PROD with MISCELLANEOUSEP01MY07.052
24042 Federal Register / Vol. 72, No. 83 / Tuesday, May 1, 2007 / Proposed Rules 

BILLING CODE 6560–50–C 

a. FDA Targeted Sampling. The FDA 

released data on perchlorate in milk, 

lettuce, and bottled water in November 

2004. To analyze food samples, FDA 

used ion chromatography (IC)-tandem 

mass spectrometry (MS/MS), referred to 

as IC–MS/MS. The quantitation limits 

for perchlorate in these analyses were 

0.5 [mu]g/L for bottled water, 1 [mu]g/ 

kg by fresh weight (FW) for lettuce, and 

3 [mu]g/L for dairy milk. The mean 

concentration of perchlorate in 128 

lettuce samples collected in 5 states 

(AZ, CA, FL, NJ, TX) was 10.3 [mu]g/kg 

FW (FDA, 2004), and ranged from not 

quantifiable (NQ) to 129 [mu]g/kg FW. 

The mean concentrations of perchlorate 

in several varieties of lettuce are 

reported in Table 4. The mean 

concentration of perchlorate in 104 

dairy milk samples collected in 14 states 

(AZ, CA, GA, KS, LA, MD, MO, NJ, NC, 

PA, SC, TX, VA, WA) was 5.76 [mu]g/ 

L (FDA, 2004), with a range from NQ to 

11.3 [mu]g/L. FDA (2004) detected 

perchlorate in 2 of the 51 bottled water 

samples representing 34 distinct sources 

collected in 12 states (CA, CO, GA, MD, 

MN, MO, NC, NE, PA, SC, TX, WI) at 

levels of 0.56 [mu]g/L and 0.45 [mu]g/ 

L. 

b. Other Published Studies. Sanchez 

(2004) and Sanchez et al. (2005a) report 

the results of an analysis of agricultural 

products sampled from the lower 

Colorado River region of Arizona and 

California, the Imperial Valley of 

California, and the Coachella Valley of 

California, where irrigation water is 

known or suspected to contain 

perchlorate. The studies were partially 

supported by the U.S. Department of 


rmajette on DSK29S0YB1PROD with MISCELLANEOUSEP01MY07.053 EP01MY07.054
Federal Register / Vol. 72, No. 83 / Tuesday, May 1, 2007 / Proposed Rules 24043 

23 Sanchez (2004) presents somewhat different 

results. Specifically, of the 44 samples of ‘‘edible 

head’’ lettuce, perchlorate was quantified in one of 

the samples (26 [mu]g/kg), perchlorate was not 

detectable in 6 samples, and the remaining 

sampling results were qualified as <MRL, which the 

author defined as ‘‘represents a seemingly 

detectable peak but below a level that can be 

quantitated.’’ 

24 A wheat kernel (seed) has three major parts— 

the bran, the germ, and the endosperm. The 

majority of the wheat kernel is the endosperm, 

which is the portion of the kernel that is retained 

in refined (white) wheat flours. Whole wheat flours 

contain endosperm, wheat bran, and wheat germ in 

approximately the same proportions as in the wheat 

kernel. Wheat flours do not contain the chaff (husk). 

Agriculture—Agricultural Research 

Service (USDA–ARS). Samples of 

iceberg, romaine, and leaf lettuce, 

carrots, onions, sweet corn, squash, 

melons, tomatoes, peppers, broccoli, 

cauliflower, cabbage, durum wheat, and 

alfalfa were analyzed for perchlorate 

using ion chromatography (IC) as the 

primary analytical method. For these 

analyses, the fresh-weight method 

reporting limit was not identified in 

most cases, but was reported to range 

from 20 to 50 [mu]g/kg FW, depending 

on the moisture content of the samples 

(Sanchez, 2004). Sanchez et al. (2005a) 

report that the method reporting level 

for iceberg lettuce was approximately 20 

[mu]g/kg FW and for other types of 

lettuce was 25–30 [mu]g/kg FW. 

Perchlorate in the irrigation water 

ranged from 1.5 to 8.0 [mu]g/L over the 

period of the survey (Sanchez et al., 

2005a). 

Sanchez et al. (2005a) analyzed 44 

samples of iceberg lettuce heads that 

had been trimmed of frame and wrapper 

leaves, which are usually removed 

before the lettuce is consumed. 

Perchlorate was quantified in 5 of the 

samples (ranging from 23 to 26 [mu]g/ 

kg FW),23 perchlorate was not detectable 

in 6 samples, and the results of the 

remaining samples were less than the 

method reporting limit, which the 

authors defined as ‘‘a detectable peak 

among duplicates and/or replicates but 

below a level that can be quantitated.’’ 

Perchlorate concentrations in 10 

samples of romaine and green leaf 

lettuce ranged from less than the 

method reporting limit to 81[mu]g/kg 

FW (Sanchez, 2004). 

As shown in Table 4, Sanchez (2004) 

also detected perchlorate in samples of 

melons, tomatoes, and peppers, but at 

levels below the method reporting limit. 

Perchlorate was not detected in carrots, 

onions, sweet corn, squash, and durum 

wheat. Concentrations of perchlorate in 

10 samples of alfalfa ranged from 109 to 

668 [mu]g/kg FW. Six of the 10 alfalfa 

samples were sent to FDA for 

confirmatory analysis by IC–MS/MS. 

The FDA results were generally lower 

than those of the corresponding samples 

by Sanchez (2004), ranging from 121 to 

382 [mu]g/kg FW. Sanchez et al. (2006) conducted 

studies to evaluate the uptake and 

distribution of perchlorate in citrus trees 

and the occurrence of perchlorate in 

lemons, grapefruit, and oranges grown 

in southern California and southwestern 

Arizona. Five whole lemon trees 

irrigated with Colorado River water 

were harvested for destructive sampling. 

Sanchez et al. (2006) estimate that the 

irrigation water had an average 

perchlorate concentration of 6 [mu]g/L. 

Most of the sample analysis was 

conducted using IC–MS/MS, having an 

MRL of approximately 25 [mu]g/kg by 

dry weight (DW). In samples of tree 

trunks, roots, and branches, perchlorate 

was close to or below the MRL. 

Perchlorate was much higher in the 

leaves than the fruit (peel and pulp), 

with mean concentrations of 1,835 and 

128 [mu]g/kg DW, respectively. Citrus samples were collected during 

2004–2005 from the lower Colorado 

River Valley, the University of Arizona 

Research Farm, the Coachella Valley, 

and Los Angeles County. All analyses of 

fruit pulp were conducted using IC–MS/ 

MS with an approximate MRL of 2.5 

[mu]g/kg FW. For the 86 citrus samples 

collected, the perchlorate concentration 

in the fruit pulp ranged from below 

detection to 37.6 [mu]g/kg FW. Mean 

concentrations in lemons (33 samples), 

grapefruit (15 samples), and oranges (28 

samples) were 2.3, 3.3, and 7.4 [mu]g/ 

kg FW, respectively. Sanchez et al. (2005b) surveyed 

perchlorate occurrence in lettuce and 

other leafy vegetables produced outside 

the lower Colorado River region. 

Samples were analyzed by IC, with a 

minimum reporting level of 

approximately 20 to 40 [mu]g/kg FW, 

depending on the leafy vegetable type. 

Results of some of the more heavily 

sampled food items are presented in 

Table 4. 

While not shown in Table 4, Sanchez 

et al. (2005b) performed additional 

analysis by partitioning the leafy 

vegetable samples by type of culture. 

Perchlorate was detected in 70 of 268 

samples of conventionally-grown leafy 

vegetables and 72 of 170 samples of 

organically-grown leafy vegetables. The 

range of perchlorate concentrations was 

ND to 104 [mu]g/kg FW in conventional 

leafy vegetables and ND to 628 [mu]g/ 

kg FW in organic leafy vegetables. 

Sanchez et al. (2005b) analyzed the 

results using regression analysis and 

estimated that the median perchlorate 

concentration in organically-grown 

samples was 2.2 times higher than in 

conventionally-grown samples. The 

regression analysis also suggested that 

variation among sampling locations was 

greater than variation among lettuce 

types. Researchers at Texas Tech University 

analyzed samples of dairy and soy milk 

using IC and/or IC/MS analytical 

methods with detection limits of 1 

[mu]g/L or better (Kirk et al., 2005). In 

a study of perchlorate in dairy milk, 

Kirk et al. (2005) found mean 

perchlorate levels of 2.0 [mu]g/L in 47 

retail dairy milk samples from 11 states 

(AK, AZ, CA, FL, HI, KS, ME, NH, NM, 

NY, PA), with a range from not detected 

(ND) to 11.0 [mu]g/L. A single sample 

of soy milk was analyzed and reported 

to contain 0.7 [mu]g/L perchlorate (Kirk 

et al., 2005). An earlier study by Kirk et 

al. (2003) found perchlorate ranging 

from 1.7 [mu]g/L to 6.4 [mu]g/L in 7 

dairy milk samples purchased in a city 

in Texas. 

Jackson et al. (2005) conducted 

limited sampling of edible and forage 

vegetation in 1 Texas county and in 1 

Kansas home garden. In Texas, wheat 

and alfalfa were sampled from 

commercial fields irrigated with 

groundwater containing perchlorate 

from an unknown source, and a 

cucumber was sampled from an 

irrigated home garden. In Kansas, 

cantaloupe, cucumber, and tomatoes 

were sampled from an irrigated home 

garden near a slurry explosives site. 

Researchers used IC for sample analysis 

but did not report fresh-weight 

detection limits. Perchlorate was 

detected in all 12 samples of winter 

wheat heads (whole, including the 

chaff) at a mean concentration of 2,000 

[mu]g/kg FW but perchlorate was not 

detected in wheat endosperm (2 

samples)24. The mean perchlorate 

concentration in 3 samples of alfalfa 

was 2,900 [mu]g/kg FW. A cucumber 

sample from a Texas home garden 

contained 40 [mu]g/kg FW perchlorate; 

a sample of irrigation water from this 

garden contained 20.7 [mu]g/L 

perchlorate. In the Kansas home garden, 

the cucumber sample contained 770 

[mu]g/kg FW perchlorate, the 

cantaloupe sample contained 1,600 

[mu]g/kg FW perchlorate, and 2 samples 

of tomato contained 42 and 220 [mu]g/ 

kg FW perchlorate. The reported 

concentration of perchlorate in 

irrigation water for the Kansas home 

garden was 81 [mu]g/L. EPA notes that 

the perchlorate levels in irrigation water 

samples associated with these two home 

gardens were significantly higher than 

in the vast majority of surface and 

ground water samples in the US. 

Aribi et al. (2006) developed an 

analytical method for perchlorate that 

uses ion chromatography with 

suppressed conductivity and 

electrospray ionization tandem mass 


rmajette on DSK29S0YB1PROD with MISCELLANEOUS
24044 Federal Register / Vol. 72, No. 83 / Tuesday, May 1, 2007 / Proposed Rules 

spectrometry (IC–ESI–MS/MS). The 

method was used to measure 

perchlorate in samples of various food 

products, including fresh/canned fruits 

and vegetables, wine, beer, and other 

beverages. Most samples were 

purchased in grocery and liquor stores 

in greater Toronto, Canada, between 

January 2005 and February 2006. 

Produce samples originated from many 

different parts of the world and all 

samples contained measurable amounts 

of perchlorate. However, the survey was 

limited to only a few samples of each 

food. Products from California, Chile, 

Costa Rica, Guatemala, and Mexico had 

the highest levels of perchlorate. 

Products from Canada and China had 

the lowest levels of perchlorate. The 

highest detection was in cantaloupe 

from Guatemala (463.50 [mu]g/kg FW). 

Analysis of raw asparagus (39.900 

[mu]g/kg FW) and cooked asparagus 

(24.345 [mu]g/kg FW) demonstrated that 

perchlorate can remain in food 

processed at a high temperature. 

Perchlorate concentrations in 8 samples 

of produce from the U.S. ranged from 

0.094 [mu]g/kg FW (for blueberries) to 

19.29 [mu]g/kg FW (for green grapes). Aribi et al. (2006) analyzed 77 

samples of wine and 144 samples of 

beer from many parts of the world. All 

samples contained measurable amounts 

of perchlorate. The wine sample with 

the single highest concentration of 

perchlorate, 50.250 [mu]g/L, was from 

Portugal. Overall, wine samples from 

Chile contained the highest 

concentrations of perchlorate, ranging 

from 5.358 to 38.88 [mu]g/L in 8 

samples. Twelve samples of wine from 

the U.S. contained perchlorate 

concentrations ranging from 0.197 to 

4.593 [mu]g/L. Results from analysis of 

beer samples varied substantially among 

countries, with an overall range from 

0.005 [mu]g/L (Ireland) to 21.096 [mu]g/ 

L (France). Concentrations of 

perchlorate in 8 beer samples from the 

U.S. ranged from 0.364 to 2.014 [mu]g/ 

L. 

Snyder et al. (2006) measured 

perchlorate in dietary supplements and 

flavor enhancing ingredients collected 

from various vendors in Las Vegas, NV, 

and Seattle, WA. Analyses were 

performed using LC–MS/MS with a 

limit of detection between 2 and 5 

[mu]g/kg. Perchlorate was detected in 

20 of 31 analyzed supplements, with 

detectable concentrations ranging from 

10 to 2,420 [mu]g/kg. Based on 

manufacturers’ recommended intake of 

the supplements, the resulting daily oral 

doses of perchlorate would range from 

0.03 to 18 [mu]g/day. Twelve of the 

supplements tested were prenatal or 

children’s vitamins. The highest level of 

perchlorate (2,420 [mu]g/kg or 0.018 

mg/day at the recommended daily dose) 

was found in a prenatal vitamin; in the 

remaining prenatal and children’s 

vitamins perchlorate did not exceed 28 

[mu]g/kg. The study noted that ‘‘vitamin 

and mineral supplements are typically 

formulated to include the 

Recommended Daily Allowance (RDA) 

of iodine, a factor that would provide 

protection against any possible impacts 

of microgram levels of perchlorate 

found in these supplements.’’ 

Perchlorate was also detected at 740 

[mu]g/kg in a sample of kelp granules (a 

flavor enhancer), which equates to 2.2 

[mu]g perchlorate per serving. Martinelango et al. (2006a) measured 

perchlorate in seaweed, which is often 

used as a source of iodide in food and 

nutritional supplements. Martinelango 

et al. (2006a) collected samples of 11 

different species of seaweed growing off 

the coast of northeastern Maine. 

Perchlorate was detected in all species, 

with concentrations ranging from 29 to 

878 [mu]g/kg DW. The iodide content in 

the samples was much higher, ranging 

from 16 to 3,134 mg/kg DW. 

Martinelango et al. (2006a) found that 

samples of Laminaria species 

concentrated iodide more selectively 

than perchlorate. Laminaria is a genus 

of large brown seaweeds that are 

commonly used in kelp tablets. 

Martinelango et al. (2006a) also 

analyzed 4 seaweed samples that had 

been washed with deionized water and 

found that a single wash removed 38 to 

73 percent of the perchlorate and 34 to 

44 percent of the iodide. 

D. Occurrence Studies on Perchlorate in 

Human Urine, Breast Milk, and 

Amniotic Fluid 

Recently researchers have used the 

results of the analysis of urine samples 

to estimate human exposure to 

perchlorate. Ingested perchlorate is not 

metabolized by humans and is excreted 

largely in the urine (Merrill et al., 2005). 

The CDC’s National Center for 

Environmental Health (NCEH) 

developed a sensitive and selective 

analytical method to analyze 

perchlorate in human urine (ValentinBlasini et al., 2005). The method uses 

ion chromatography coupled with 

electrospray ionization tandem mass 

spectrometry (IC/MS/MS) and achieves 

an MRL of 0.025 [mu]g/L in human 

urine. The authors report that the 

method is robust enough to process 

first-morning-void urine samples, which 

are samples of the first voiding of urine 

upon waking. Valentin-Blasini et al. (2005) analyzed 

urine samples from 61 healthy adult 

donors who lived in the area of Atlanta, 

Georgia. The urine samples were 

provided anonymously, without 

associated donor information. 

Perchlorate was detected in all of the 

urine samples, with concentrations 

ranging from 0.66 to 21 [mu]g/L. The 

authors cited dietary exposure as a 

potential source of perchlorate because 

perchlorate was found only at low levels 

(0.1—0.2 [mu]g/L) in area tap water 

samples (Valentin-Blasini et al., 2005). 

Valentin-Blasini et al. (2005) also 

analyzed the urine samples for 

creatinine, which is a metabolic 

breakdown product in muscles that is 

eliminated from the body in urine at a 

predictable rate. When adjusted for 

urinary creatinine content, the reported 

range of perchlorate in the samples is 

1.0 to 35 [mu]g of perchlorate per gram 

of creatinine. The median perchlorate 

concentration was 3.2 [mu]g/L (7.8 

[mu]g/g creatinine). The researchers 

stated that only 1 sample from the 

Atlanta population contained 

perchlorate at a level slightly in excess 

of the amount expected to be excreted 

by an individual exposed to perchlorate 

at the reference dose of 0.0007 mg/kg/ 

day (Valentin-Blasini et al., 2005). 

Specifically, assuming that perchlorate 

is excreted uniformly in urine 

throughout the day, a urinary excretion 

level of 34 [mu]g perchlorate per gram 

creatinine would be associated with a 

daily perchlorate intake of 0.0007 mg/ 

kg/day, for a 70 kg male that excretes 

creatinine at a typical rate of 1.44 grams 

per day (g/day). These assumptions are 

imprecise for individual exposure 

assessment but allow for spot urine 

perchlorate excretion to be related to the 

reference dose for toxicological 

perspective. Estimating perchlorate 

exposure from a single spot urine 

sample (as opposed to a sample 

collected continuously over a period of 

time) is imprecise due to the episodic 

nature of perchlorate exposure and the 

short half-life of perchlorate in the 

human body. The precision of estimated 

individual perchlorate exposure can be 

improved by more precise estimation of 

24-hour creatinine excretion based on 

sex, height, weight, and age as described 

by Mage et al. (2004). In addition, 

imprecision stemming from the episodic 

nature of perchlorate exposure can be 

reduced with increased sampling. 

The analytical method developed by 

Valentin-Blasini et al. (2005) was 

further used by Blount et al. (2006a) to 

evaluate urine samples from 27 

volunteers with differing dietary habits. 

Blount et al. (2006a) collected firstmorning-void urine specimens from 

volunteers living in the Atlanta area. 

The study volunteers self-assessed their 

consumption of milk, dairy products, 

and green/leafy vegetables within the 16 

hours before the sample was collected. 


rmajette on DSK29S0YB1PROD with MISCELLANEOUS
Federal Register / Vol. 72, No. 83 / Tuesday, May 1, 2007 / Proposed Rules 24045 

The samples were grouped into 2 

categories (‘‘one or fewer servings’’ and 

‘‘three or more servings’’) based on total 

consumption of these selected foods. 

Total daily perchlorate exposure was 

calculated using a bodyweight of 70 kg 

and a creatinine excretion rate of 1.44 g/ 

day, assuming that each first-morning 

void urine sample was representative of 

that individual’s daily perchlorate 

exposure. Each volunteer also collected 

a drinking water sample from home and 

work. Blount et al. (2006a) analyzed 

drinking water samples with the same 

method used for urine analysis and 

estimated exposure from drinking water 

based on a body weight of 70 kg and 

daily consumption of 2 liters of water 

per day. The mean creatinine-adjusted 

urinary perchlorate level was 1.8 times 

higher for individuals who identified 

themselves as consuming three or more 

servings of milk, dairy products, and/or 

green/leafy vegetables (6.13 versus 3.45 

[mu]g/g creatinine). There were no 

significant differences in the perchlorate 

levels in the drinking water samples of 

the 2 diet groups, which ranged from 

<0.05 to 0.25 [mu]g/L with a median of 

0.10 [mu]g/L. Using a median drinking 

water level of 0.10 [mu]g/L, Blount et al. 

(2006a) estimated that the perchlorate 

dose from drinking water was 0.003 

[mu]g/kg/day. Compared to this 

drinking water estimate, the total 

perchlorate dose estimate based on 

mean urinary perchlorate excretion was 

24 times higher (0.071 [mu]g/kg/day) 

and 42 times higher (0.126 [mu]g/kg/ 

day) for the low-consumption and highconsumption diet groups, respectively. 

The overall range of perchlorate found 

in urine was 0.94 to 17 [mu]g/g 

creatinine with a median of 4.2 [mu]g/ 

g creatinine. In the largest study of its kind, Blount 

et al. (2006c) measured perchlorate in 

urine samples collected from a 

nationally representative sample of 

2,820 U.S. residents, ages 6 years and 

older, as part of the 2001–2002 

NHANES. Blount et al. (2006c) detected 

perchlorate at concentrations greater 

than 0.05 [mu]g/L in all 2,820 urine 

samples tested, with a median 

concentration of 3.6 [mu]g/L (3.38 

[mu]g/g creatinine) and a 95th 

percentile of 14 [mu]g/L (12.7 [mu]g/g 

creatinine). Only 0.7% of the study 

participants had an estimated 

perchlorate dose in excess of 0.0007 mg/ 

kg/day. Women of reproductive age (15– 

44 years) had a median urinary 

perchlorate concentration of 2.9 [mu]g/ 

L (2.97 [mu]g/g creatinine) and a 95th 

percentile of 13 [mu]g/L (12.1 [mu]g/g 

creatinine). The demographic with the 

highest concentration of urinary 

perchlorate was children (6–11 years), 

who had a median urinary perchlorate 

concentration of 5.2 [mu]g/L (5.79 

[mu]g/g creatinine). Blount et al. (2006c) 

estimated a total daily perchlorate dose 

for each adult and found a median dose 

of 0.066 [mu]g/kg/day (about one tenth 

of the RfD) and a 95th percentile of 

0.234 [mu]g/kg/day (about one third of 

the RfD). Eleven adults (0.7%) had 

estimated perchlorate exposure in 

excess of the RfD (0.7 [mu]g/kg/day). 

The highest estimated exposure was 

3.78 [mu]g/kg/day. Because of daily 

variability in diet and perchlorate 

exposure, and the short residence time 

of perchlorate in the body, these single 

sample measurements may overestimate 

long-term average exposure for 

individuals at the upper end of the 

distribution and may underestimate the 

long-term average exposure for 

individuals at the lower end of the 

distribution. Daily perchlorate dose is 

not presented for children and 

adolescents due to the limited 

validation of formulas for these age 

groups (Blount et al., 2006c). 

Valentin-Blasini et al. (2005) and 

T[eacute]llez et al. (2005) analyzed 

urine samples of pregnant women in 3 

cities in Chile and found higher median 

levels of urinary perchlorate in cities 

with higher concentrations of 

perchlorate in tap water. Based on an 

assessment of drinking water intake, the 

researchers determined that, in all 3 

cities, there was an additional source of 

perchlorate for the study participants 

that may be explained by dietary (food) 

intake (T[eacute]llez et al., 2005). This 

gap between estimated perchlorate 

exposure and perchlorate intake from 

tap water consumption ranged from 21.7 

[mu]g/day to 33.8 [mu]g/day in the 3 

Chilean cities (T[eacute]llez et al., 

2005). 

Martinelango et al. (2006b) developed 

a method to measure perchlorate in 

human urine with a limit of detection of 

0.080 [mu]g/L, and reported analytical 

results of 9 spot urine samples from 

male and female volunteers. Perchlorate 

was present in all samples analyzed, at 

concentrations ranging from 2.2 to 14.9 

[mu]g/L, with a median value of 8.1 

[mu]g/L. Other studies have investigated 

perchlorate in human breast milk. Kirk 

et al. (2005) analyzed 36 breast milk 

samples from 18 states (CA, CT, FL, GA, 

HI, MD, ME, MI, MO, NC, NE, NJ, NM, 

NY, TX, VA, WA, WV) and found 

perchlorate concentrations in all 

samples ranging from 1.4 to 92.2 [mu]g/ 

L in all samples, with a mean 

concentration of 10.5 [mu]g/L. 

T[eacute]llez et al. (2005) report 

maternal parameters for participants 

from the study in Chile. Breast milk 

samples indicated that a significant 

amount of perchlorate leaves the body 

of the nursing mother through breast 

milk, in addition to urine. However, the 

breast milk perchlorate levels were 

highly variable and no significant 

correlations could be established 

between breast milk perchlorate and 

either urine perchlorate or breast milk 

iodide concentrations for the 

individuals evaluated in these Chilean 

cities (T[eacute]llez et al., 2005). Kirk et 

al. (2006) evaluated variations of iodide, 

thiocyanate and perchlorate in human 

milk samples. These authors suggest 

that if the overall intake of iodide is 

sufficient, it is unlikely that milk with 

an occasional low iodide or high 

perchlorate content would pose a major 

risk to infants. However, their limited 

data (evaluating only 10 women) show 

that the milk of some women may not 

supply infants with adequate iodide and 

they suggest that it may be important to 

base risk assessments for perchlorate 

exposure on the iodide to perchlorate 

ratio or the ratio of iodide to a 

‘‘selectively-weighted sum of iodide 

uptake inhibiting agents.’’ 

Blount and Valentin-Blasini (2006) 

developed a sensitive and selective 

method for quantifying iodide, 

perchlorate, thiocyanate, and nitrate in 

human amniotic fluid. The analytical 

limit of detection for perchlorate was 

calculated to be 0.020 [mu]g/L. Samples 

of amniotic fluid at 15 to 20 weeks 

gestation were collected from 48 healthy 

women in an Eastern U.S. city for 

analysis. Perchlorate was found in all 

samples tested and exhibited a lognormal distribution. The perchlorate 

concentrations ranged from 0.057 to 

0.71 [mu]g/L with a median value of 

0.18 [mu]g/L. 

E. Status of the Preliminary Regulatory 

Determination for Perchlorate 

As stated earlier, the Agency is not 

making a preliminary regulatory 

determination for perchlorate in this 

notice. The Agency believes that 

additional information is needed on the 

sources of human exposure if it decides 

to base its determination regarding 

health risk reduction potential on a 

health reference level (HRL) derived 

from the RfD and the relative source 

contribution (RSC) for drinking water. 

Under this approach, the Agency would 

use the RfD and RSC to estimate an HRL 

and then use this HRL as a benchmark 

against which to conduct an evaluation 

of the occurrence data. In conducting 

such an assessment for the 6 noncarcinogens discussed previously in this 

action, EPA used a 20 percent RSC, 

which is the lowest and most 

conservative RSC used to estimate an 

HRL. Since the initial screening of the 

occurrence data against the HRL 

resulted in a preliminary negative 

determination, the Agency found that it 


rmajette on DSK29S0YB1PROD with MISCELLANEOUS
24046 Federal Register / Vol. 72, No. 83 / Tuesday, May 1, 2007 / Proposed Rules 

25 Massachusetts promulgated a final drinking 

water standard of 2 [mu]g/L for perchlorate on July 

28, 2006. For more information about the final 

standard, see http://www.mass.gov/dep/public/ 

press/pchl0706.htm (MA DEP, 2006). 

was not necessary to further evaluate 

the RSC for these contaminants. In the 

case of perchlorate, the Agency is not at 

the point of being able to make either a 

negative or a positive determination 

using this approach because it is not yet 

clear what an appropriate RSC for 

perchlorate is. If EPA were to use a 

default RSC of 20% for perchlorate, the 

resulting HRL would be 5 [mu]g/L. 

Approximately 3.16% of the 3,858 

PWSs in the UCMR1 data set had at 

least one detect of perchlorate greater 

than or equal to 5 [mu]g/L. Given this 

level of occurrence at the defaultderived HRL, the Agency believes a 

better informed RSC and HRL would be 

needed to use this approach to 

determine whether regulation of 

perchlorate in drinking water presents a 

meaningful opportunity for health risk 

reduction. 

Table 5 shows the number of systems 

and population served that would 

exceed the HRL under various RSC 

scenarios and the sensitivity of this 

estimate to relatively small changes in 

the estimated RSC. For example, 

increasing the RSC from 20 to 30 

percent would lower the estimated 

number of systems impacted by about a 

third and the estimated population 

served by about half. Hence, the choice 

of an appropriate RSC and resulting 

HRL could impact EPA’s determination 

of whether regulation of perchlorate 

represents a meaningful opportunity for 

health risk reduction if it uses this 

approach. 

EPA recognizes that system-level 

population estimates shown in Table 5 

may be conservative because some 

systems have multiple entry points to 

the distribution system and not all entry 

points had a positive detection for 

perchlorate in the UCMR 1 survey. 

Hence, to derive a less conservative 

population estimate (last column in 

Table 5), EPA assumed that the 

population for each system is equally 

distributed over all of the entry (or 

sampling) points and estimated a 

population-served value based on entry 

points that had at least 1 analytical 

detection for perchlorate at levels 

greater than each of the HRL thresholds. 

TABLE 5.—UCMR 1 OCCURRENCE AND POPULATION ESTIMATES FOR PERCHLORATE AT VARIOUS HRL THRESHOLDS a

RSC scenarios 

(percent) 

Estimated HRL thresholds based on various 

RSC scenarios b

PWSs with at least 1 

detection ≤ threshold of 

interest 

PWS entry or sample 

points with at least 1 

detection ≤ threshold of 

interest c

Population 

served by 

PWSs with at 

least 1 detection ≤ threshold of interest d

Population 

estimate for 

entry or sample points having at least 1 

detection ≤ 

threshold of 

interest e

20 ..................................... 5 [mu]g/L ......................... 3.16% (122 of 3,858) ...... 1.88% (281 of 14,984) .... 14.6 M 4.0 M 

30 ..................................... 7 [mu]g/L ......................... 2.13% (82 of 3,858) ........ 1.14% (171 of 14,984) .... 7.2 M 2.2 M 

40 ..................................... 10 [mu]g/L ....................... 1.35% (52 of 3,858) ........ 0.65% (97 of 14,984) ...... 5.0 M 1.5 M 

50 ..................................... 12 [mu]g/L ....................... 1.09% (42 of 3,858) ........ 0.42% (63 of 14,984) ...... 3.6 M 1.2 M 

60 ..................................... 15 [mu]g/L ....................... 0.80% (31 of 3,858) ........ 0.29% (44 of 14,984) ...... 2.0 M 0.9 M 

70 ..................................... 17 [mu]g/L ....................... 0.70% (27 of 3,858) ........ 0.24% (36 of 14,984) ...... 1.9 M 0.8 M 

80 ..................................... 20 [mu]g/L ....................... 0.49% (19 of 3,858) ........ 0.16% (24 of 14,984) ...... 1.5 M 0.7 M 

100 ................................... 25 [mu]g/L ....................... 0.36% (14 of 3,858) ........ 0.12% (18 of 14,984) ...... 1.0 M 0.4 M 

Footnotes: 

a These data represent summary statistics for the 3,858 public water systems that have sampled for perchlorate as a part of the UCMR 1 survey. b HRL threshold = [(RfD of 0.0007 mg/kg/day x 70 kg BW for pregnant female) / (2 L DWI)] x the RSC scenario. Each HRL threshold value is 

converted from mg/L to [mu]g/L units and then rounded to the nearest whole number. c The entry/sample-point-level population served estimate is based on the system entry/sample points that had at least 1analytical detection for 

perchlorate greater than the HRL threshold of interest. The UCMR 1 small system survey was designed to be representative of the nation’s small 

systems, not necessarily to be representative of small system entry points. d The system-level population served estimate is based on the systems that had at least 1analytical detection for perchlorate greater than the 

HRL threshold of interest. e Because the population served by each entry/sample point is not known, EPA assumed that the total population served by a particular system is equally distributed across all entry/sample points. To derive the entry/sample point-level population estimate, EPA summed the population 

values for the entry/sample points that had at least 1 analytical detection greater than the threshold of interest. 

Table 5 also includes information on 

the effects of using an RSC of 100% 

(that is, using an HRL set at the DWEL 

of 24.5 [mu]g/L, rounded to a whole 

number). Crawford-Brown et al. (2006), 

in an estimate of risk variability from 

perchlorate exposure through 

community water systems, noted that 

the subjects in the original 2002 Greer 

et al., study (on which the RfD of .0007 

mg/L was based) presumably had other 

sources of perchlorate exposure outside 

of the study and suggested that it may 

be appropriate to view their results as 

reflecting the effects of incremental 

exposure to perchlorate above the 

background levels already in food and 

water rather than the effects of total 

exposure, as is implicitly assumed when 

the HRL is derived using an RSC to 

account for other sources of exposure. 

Use of an RSC to derive the HRL is 

clearly appropriate when the RfD or 

cancer slope factor is derived from 

animal studies with carefully controlled 

exposure. Crawford-Brown et al. 

suggest, however, that an RSC is not 

necessary for perchlorate because there 

is no reason to assume that the 

background exposure of the study 

subjects was different than that of the 

general population. EPA notes that the 

sample size in the Greer study was 

small and EPA is not aware of data on 

their background exposure to 

perchlorate or how representative it may 

be. EPA requests comment on whether 

information is available on the 

background exposure of subjects in the 

Greer study and whether it should 

consider the background exposure of 

these subjects in determining an HRL 

for perchlorate. 

While several States have 

recommended guidelines or public 

health goals for perchlorate, EPA 

recognizes that at least 1 state, 

Massachusetts,25 has already 

promulgated a final drinking water 

standard for perchlorate, that other 

States may set drinking water standards 

in the future, and that these standards 


rmajette on DSK29S0YB1PROD with MISCELLANEOUS
Federal Register / Vol. 72, No. 83 / Tuesday, May 1, 2007 / Proposed Rules 24047 

26 Information about FDA’s TDS design, food list, 

analytes, and analytical results can be found at 

http://www.cfsan.fda.gov/comm/tds-toc.html. 

(FDA, 2006) 

could impact national occurrence 

estimates once these standards are fully 

implemented. 

F. What Are the Potential Options for 

Characterizing Perchlorate Exposure 

and Proceeding With the Preliminary 

Regulatory Determination for 

Perchlorate? 

While the Agency recognizes that 

food and other pathways may be 

important sources of perchlorate 

exposure, the Agency believes the 

currently available food data 

(summarized in section V.C.3) are 

inadequate to develop a better informed 

RSC (and HRL). First, some of the 

existing data are limited in their sample 

numbers, geographic coverage, and 

analytical method adequacy. Second, 

the current studies provide little or no 

data for several food groups (e.g., meat, 

poultry, fish, eggs, root and tuber 

vegetables, brassica vegetables, bulb 

vegetables, tree fruits, legumes, and 

cereal grains) that account for about half 

of the diet (by mass) for females of 

reproductive age (mid-teens to midforties). 

This section presents and requests 

comment on data EPA might use to 

estimate an RSC based on food-borne 

exposure as well as on several other 

options that the Agency is considering 

to better characterize perchlorate 

exposure and assist the Agency in 

making its regulatory determination for 

perchlorate. These options could serve 

as a supplement or an alternative to 

developing an HRL based on a better 

informed RSC derived from food 

concentration and consumption data. 

The Agency specifically seeks comment 

on the use of urine biomonitoring data 

in estimating perchlorate exposure. If 

the Agency decides to use any of the 

approaches discussed in V.F.2, EPA will 

need to determine what statistics (e.g., 

mean, median, percentile, etc.) are most 

appropriate for consideration in a 

regulatory determination. The Agency 

will also conduct a peer review, as 

appropriate, of any new methodology it 

decides to use. 

The Agency also invites the public to 

submit relevant data that may further 

characterize exposure to perchlorate 

through consumption of foods and/or 

through other pathways. The Agency 

will consider any new, relevant 

information/data provided in response 

to this action as the Agency determines 

whether to regulate perchlorate with a 

national primary drinking water 

regulation. 1. Use of Food Concentration and 

Consumption Data to Estimate an RSC. 

In the past, the Agency has relied on 

dietary exposure information from the 

FDA Total Diet Study (TDS) to 

determine the RSC allowed for drinking 

water and to set health goals (i.e., 

Maximum Contaminant Level Goals) for 

several inorganic compounds (e.g., 

antimony, cadmium, chromium, and 

selenium). Under the TDS, foods are 

sampled at retail outlets, prepared as 

they would be consumed, and analyzed 

for a variety of analytes (e.g., nutrients, 

pesticides, industrial chemicals). 

Approximately 280 foods, covering a 

broad spectrum of the diet, are currently 

sampled in each sampling event. 

Sampling events (known as ‘‘market 

baskets’’) occur about 4 times per year, 

with each event being confined to 1 of 

the 4 regions of the country. The dietary 

intake of the analyzed compounds can 

be calculated for the U.S. population by 

multiplying the concentrations found in 

TDS foods by the consumption amounts 

for each food. FDA compiles food 

consumption amounts for the total U.S. 

population by gender and by age 

group.26

FDA is including perchlorate as an 

analyte in the 2006 TDS. EPA believes 

that a comprehensive dietary intake 

estimate for perchlorate will be useful in 

evaluating dietary exposure relative to 

drinking water. When sufficient 

quantitative exposure data are available 

(such as the data published by FDA in 

conjunction with the TDS), EPA can use 

the procedure used previously for 

several regulated inorganic compounds 

(i.e., chromium and selenium) to 

calculate the relative source 

contribution for perchlorate. In these 

cases where dietary intake values were 

available, EPA subtracted the dietary 

intake value from the Drinking Water 

Equivalent Level DWEL and used the 

remainder as the allowance for water. 

This procedure assures that total 

exposure does not exceed the RfD. The Agency invites the public to 

submit relevant data that may further 

characterize exposure to perchlorate 

through consumption of foods and/or 

through other pathways. This 

information may help the Agency in the 

evaluation of currently available food 

data and the 2006 TDS. 

2. Use of Urinary Biomonitoring Data 

to Evaluate Exposure to Perchlorate. 

Researchers at CDC’s National Center for 

Environmental Health (NCEH) have 

conducted a large national study of total 

perchlorate exposure through analysis 

of urine samples collected for NHANES 

2001–2002 (Blount et al., 2006b and 

2006c). The use of urinary perchlorate 

excretion to estimate perchlorate 

exposure has been demonstrated in 

Valentin-Blasini et al. (2005), Tollez et 

al. (2005), and Blount et al. (2006c). 

While this would be the first time the 

Agency has used biomonitoring data to 

assist EPA in making a preliminary 

regulatory determination for a CCL 

contaminant, the Agency believes that 

estimating perchlorate exposure among 

large populations using urinary 

perchlorate excretion data may be 

appropriate for the following reasons: 

<bullet≤ Perchlorate is not 

metabolized in the body and is excreted 

unchanged primarily via the renal 

pathway (Merrill et al., 2005), 

<bullet≤ Perchlorate does not 

bioaccumulate, that is, it is excreted 

essentially completely (Merrill et al., 

2005), 

<bullet≤ Perchlorate has a short halflife in the human body (approximately 

8 hours), simplifying the estimation of 

daily exposure (Greer et al., 2002), and 

<bullet≤ A methodology exists that 

allows estimation of daily perchlorate 

intake from all sources (e.g., water, food) 

using standard creatinine adjustment 

factors to account for variations in urine 

concentration (Mage et al., 2004). 

The Agency could use the 2001–2002 

NHANES urine data in several ways as 

described in the following paragraphs. 

The Agency welcomes comment from 

the public on these approaches, as well 

as suggestions for other analyses that 

may inform the preliminary regulatory 

determination for perchlorate. 

One potential approach is to use the 

2001–2002 NHANES urine data to 

directly determine whether regulation of 

perchlorate in drinking water presents a 

meaningful opportunity for health risk 

reduction. More specifically, we could 

use the urine data (as in Blount et al., 

2006b and c) to evaluate whether total 

exposure from food and water is likely 

to result in an appreciable risk of 

adverse health effects for the U.S. 

population. If the Agency concluded 

that total exposure, as estimated from 

the urine data, does not pose an 

appreciable risk, even at the upper end 

of the exposure distribution, then it 

would follow logically that reducing 

this exposure by regulating drinking 

water would not present a meaningful 

opportunity for health risk reduction. 

As summarized above, Blount et al. 

(2006c) estimated a median total daily 

perchlorate dose for adults of 0.066 

[mu]g/kg/day (about one tenth of the 

RfD) and a 95th percentile dose of 0.234 

[mu]g/kg/day (about one third of the 

RfD). Only eleven adults (0.7%) had an 

estimated dose in excess of the RfD (0.7 

[mu]g/kg/day). EPA requests comment 

on whether or not these data provide an 

adequate basis to support a regulatory 


rmajette on DSK29S0YB1PROD with MISCELLANEOUS
24048 Federal Register / Vol. 72, No. 83 / Tuesday, May 1, 2007 / Proposed Rules 

determination for perchlorate. EPA also 

requests comment on the relevance, if 

any, to a regulatory determination for 

perchlorate, of the Blount et al (2006b) 

study, which showed an association 

between T4/TSH levels in women and 

urinary perchlorate concentrations at 

levels below the RfD (see Section V.B). 

EPA could also use the 2001–2002 

NHANES urine data to qualitatively 

evaluate the importance of the water 

contribution to overall exposure. For 

this approach, the Agency could merge 

data from the 2001–2002 NHANES and 

UCMR 1 and compare the total 

perchlorate exposure values (based on 

the urine data) for the population of 

individuals whose drinking water 

contains perchlorate at various 

concentration levels, ranging from nondetect to the upper end of the 

occurrence distribution. The intent of 

this analysis would be to permit the 

Agency to determine whether total 

perchlorate exposure (as measured in 

urine) is meaningfully correlated with 

concentrations in local public drinking 

water supplies, though EPA would only 

use these results qualitatively because it 

is not possible to match up individual 

urine samples with individual drinking 

water exposures. However, the results 

could be useful in determining at least 

qualitatively the potential significance 

of drinking water exposure for total 

exposure. If there were not a significant 

correlation between public water system 

perchlorate occurrence and individual 

exposure as measured through 

biomonitoring, this might suggest that 

there is not a meaningful opportunity 

for health risk reduction through 

regulation of drinking water. 

The Agency could also potentially use 

the 2001–2002 NHANES urine data to 

derive an RSC to use for drinking water. 

This could potentially be done in 

several different ways as follows. 

a. Use of Urinary Biomonitoring Total 

Exposure Value to Estimate an RSC. 

One possible approach to estimating an 

RSC for water would be to use the urine 

data to estimate total perchlorate 

exposure, then subtract this exposure 

value from the reference dose and allow 

the remainder as the exposure limit for 

water. The allowed remainder divided 

by the RfD would be the RSC for 

drinking water. This approach would 

yield a conservative RSC value because 

the exposure used to represent food 

would actually correspond to both food 

and drinking water exposure, whereas, 

if it were possible to estimate the 

exposure from food alone, the relative 

amount allowed for water would be 

larger (resulting in a higher RSC and 

higher health reference value). As 

discussed in Section V.D, Blount et al. 

(2006c) estimated a total daily 

perchlorate dose for adults from urine 

data and found a median dose of 0.066 

[mu]g/kg/day (about one tenth of the 

RfD) and a 95th percentile of 0.234 

[mu]g/kg/day (about one third of the 

RfD). If EPA were to use the estimated 

95th percentile total dose from the 

Blount study as if it represented the 

exposure from food alone, this would 

suggest a residual screening-level RSC 

of about 70% allocated to water. One 

possible limitation of this approach is 

that the Blount study estimates 

exposure for adults only. Therefore, an 

RSC developed based upon this data 

would not necessarily be representative 

of children. EPA requests comment on 

using this approach as the basis for 

deriving a screening-level RSC. 

b. Use of the Urine Data and UCMR 

1 to Deduce Exposure from Other 

Sources and Derive the RSC. 

Alternately, for those NHANES survey 

subjects served by public drinking water 

systems with positive detections for 

perchlorate (based on UCMR 1), EPA 

could estimate the expected perchlorate 

dose contributed by drinking water 

(using individual water consumption 

data from the NHANES survey 

combined with UCMR 1 data for the 

area in which they live) and subtract it 

from the total perchlorate dose (based 

on urinary perchlorate excretion data) to 

calculate the amount contributed by 

food. Subtraction of this calculated food 

contribution from the RfD would yield 

the amount allowed for drinking water, 

which could be divided by the RfD to 

calculate an RSC. One limitation of this 

methodology would be the assumption 

that subjects in the NHANES study are 

uniformly consuming drinking water 

that contains perchlorate at the 

concentration indicated in the UCMR 1 

data for their area. 

c. Use of Urinary Biomonitoring Data 

from Exclusive Bottled Water Drinkers 

to Estimate an RSC. The 2001–2002 

NHANES data includes urinary 

perchlorate data for populations who 

exclusively drink bottled water. As 

noted in section V.C.3.a, FDA (2004) 

tested 51 samples of bottled water from 

34 distinct sources in 12 states and 

detected perchlorate in 2 samples (at 

levels of 0.56 [mu]g/L and 0.45 [mu]g/ 

L). These levels are well below the MRL 

for the UCMR 1 data and would not 

contribute significant amounts of 

perchlorate relative to the RfD. If the 

population of exclusive bottled water 

drinkers is sufficiently representative of 

the U.S. population, these data 

potentially could be used to estimate the 

contribution of perchlorate exposure 

coming from food and allow the Agency 

to estimate an RSC for drinking water. 

The RSC value could be derived by 

subtracting the estimated perchlorate 

exposure for exclusive bottled water 

drinkers from the RfD of 0.0007 mg/kg/ 

day, using the remainder as the 

allowance for drinking water. One 

limitation of this methodology is that 

the perchlorate concentration of the 

bottled water used by this NHANES 

population is not known. Hence, we 

would have to assume that the bottled 

water concentration data collected by 

FDA (2004) is representative of the 

perchlorate concentration in the bottled 

water used by the NHANES exclusive 

bottled water population. Another 

limitation of this approach is that it 

would not subtract out the fraction of 

the drinking water intake that comes 

from water used for cooking purposes 

(since bottled water is probably not used 

by most subjects in cooking and 

household food preparation). It would 

thus produce a conservative (health 

protective) estimate of the RSC as it 

would overestimate the fraction of total 

exposure coming from food. 

G. Next Steps 

After the Agency evaluates and 

thoroughly reviews public comments 

and any new information/data on 

perchlorate obtained following this 

notice, and performs the necessary 

analyses, the Agency intends to move 

expeditiously to publish a preliminary 

regulatory determination for 

perchlorate. Depending on how quickly 

the Agency is able to complete the 

necessary analyses and determine the 

best approach for making this 

determination, EPA may be able to 

publish the preliminary determination 

in time to include a final determination 

for perchlorate as part of the final CCL 

2 regulatory determination, which is 

due by July, 2008. If not, the Agency 

will publish its final determination for 

perchlorate as soon thereafter as 

possible. EPA does not intend to wait 

until the CCL 3 regulatory 

determination cycle to complete its 

determination for perchlorate. 

VI. What About the Remaining CCL 2 

Contaminants? 

As previously stated, EPA is only 

making regulatory determinations on 

CCL 2 contaminants that have sufficient 

information to support a regulatory 

determination at this time. Section V 

discusses the status of EPA’s review of 

perchlorate. For the 30 remaining 

chemicals and the 9 microbial 

pathogens, the Agency lacks adequate 

information in the areas of health effects 

or occurrence or both. 

The Agency continues to conduct 

research and/or to collect information 


rmajette on DSK29S0YB1PROD with MISCELLANEOUS
Federal Register / Vol. 72, No. 83 / Tuesday, May 1, 2007 / Proposed Rules 24049 

on the remaining CCL 2 contaminants to 

fill identified data gaps. Stakeholders 

may be concerned that regulatory 

determinations for such contaminants 

should not necessarily wait until the 

end of the next regulatory determination 

cycle. In this regard, it is important to 

recognize that the Agency is not 

precluded from conducting research, 

monitoring, developing guidance or 

health advisories, and/or making a 

determination prior to the end of the 

next cycle. In addition, the Agency is 

not precluded from regulating a 

contaminant at any time when it is 

necessary to address an urgent threat to 

public health, including any 

contaminant not listed on the CCL. 

Because the focus of this action is to 

announce and solicit public comment 

on the Agency’s preliminary 

determinations for 11 of the 51 CCL 2 

contaminants, this action primarily 

provides information on these 11 

contaminants. The Agency recognizes 

that the public may have a particular 

interest in metolachlor, methyl tertiary 

butyl ether (MTBE), and the microbial 

contaminants. Therefore, this action 

includes some additional information 

for these contaminants in the following 

sections and requests public comment 

on any further data, information and/or 

analyses that the Agency should be 

aware of. 

A. Metolachlor 

1. Background. Metolachlor is a broad 

spectrum herbicide used for general 

weed control in many agricultural food 

and feed crops (primarily corn, 

soybeans and sorghum), on lawns and 

turf, ornamental plants, trees, shrubs 

and vines, rights of way, fencerows and 

hedgerows, and in forestry. Metolachlor 

appears to be moderately persistent to 

persistent and depending on the type of 

soil, can be highly mobile. Degradation 

of metolachlor in the environment is 

dependent on microbially-mediated and 

abiotic processes. Metolachlor has at 

least 5 major degradates. Two of the 

more common degradates are 

metolachlor ethane sulfonic acid (ESA) 

and metolachlor oxanilic acid (OA). 

2. Health. The Agency established an 

RfD for metolachlor of 0.1 mg/kg/day 

based on an NOAEL of 9.7 mg/kg/day 

and a UF of 100 (USEPA, 1995). The 

Agency derived the NOAEL from a oneyear chronic feeding study in beagle 

dogs where the critical effect was 

decreased body weight gain. 

Metolachlor shows some evidence of 

causing developmental toxicity effects 

in rats but none in rabbits. The doses 

associated with the developmental 

effect in rats are greater than the NOAEL 

and therefore the NOAEL would be 

protective against developmental 

toxicity. Metolachlor has been evaluated for 

carcinogenic activity in both rats and 

mice. No treatment-related cancer 

effects were observed in 2 studies using 

mice. In studies using rats, metolachlor 

caused a significant increase in liver 

nodules and carcinomas in high dose 

females. Negative results from 

mutagenicity studies suggest that 

tumors may result from a nonmutagenic 

mode of action. In 1991, a peer review 

committee recommended that 

metolachlor be classified as a possible 

human carcinogen based on increases in 

liver tumors in the female rat. However, 

a peer review conducted in July 1994 

recommended that the evidence for 

cancer was suggestive and should not be 

quantified. This recommendation was 

supported by negative mutagenicity data 

and recent metabolism data indicating 

that the formation of the metabolite 

presumed to be the ultimate carcinogen 

is very low (USEPA, 1995). 3. Occurrence. EPA included 

metolachlor as an analyte in the UCM 

Round 2 survey. EPA evaluated the 

UCM Round 2 Cross Section data and 

found that metolachlor was detected at 

or above the reporting limit of 0.1 

[mu]g/L in 0.83% of the 12,953 systems 

that sampled for metolachlor (USEPA, 

2006a). 

The USGS NAWQA program included 

metolachlor as an analyte in its 1992– 

2001 monitoring survey of ambient 

surface and ground waters across the 

United States. EPA evaluated the results 

of the provisional data, which are 

available on the Web at http:// 

ca.water.usgs.gov/pnsp/ (Martin et al., 

2003; Kolpin and Martin, 2003). While 

the USGS detected metolachlor in both 

surface and ground waters, 95 percent of 

the samples from the various land use 

settings were less than 1.38 [mu]g/L. 

The maximum surface water 

concentration is 77.6 [mu]g/L 

(agricultural setting) and the maximum 

estimated ground water concentration is 

32.8 [mu]g/L (agricultural setting). 4. Consideration of the ESA and OA 

degradates. While EPA has health and 

occurrence information for metolachlor 

itself, the Agency believes it is prudent 

to also consider the occurrence and 

exposure of the ESA and OA degradates 

as well. At this time, there is no finished 

water occurrence and exposure 

information for these 2 degradates from 

a nationally representative sample of 

PWSs. However, a few small-scale 

studies indicate that the ESA and the 

OA degradates may be occurring at 

greater frequencies and at higher 

concentrations than the metolachlor 

parent (Phillips et al., 1999a and 1999b; 

Rheineck and Postle, 2000). In order to 

gather more information about the 

occurrence of the ESA and OA 

degradates in finished water (along with 

the metolachlor parent), the Agency has 

added these degradates and their parent 

to the second unregulated contaminant 

monitoring regulation (UCMR 2; 70 FR 

49093; USEPA, 2005g). While EPA 

awaits the results of the UCMR 2 survey, 

the Agency is planning to update the 

health advisory for metolachlor to 

include the ESA and OA degradates. 

The Agency requests comment from the 

public as to whether updating the health 

advisory to include these degradates 

will be useful for States and public 

water utilities. 

In addition, the Agency requests 

answers to the following questions and 

any available data: 

<bullet≤ Are States collecting data on 

the co-occurrence of metolachlor and its 

degradates in source waters on a statewide basis? In drinking water on a statewide basis? 

<bullet≤ If available, are States willing 

to provide data on the co-occurrence of 

metolachlor and its ESA and OA 

degradates in community and public 

water systems? What analytical method 

and reporting limit were used to gather 

these data? 

<bullet≤ Do States have any 

information on the number of PWSs 

impacted by metolachlor and/or its 

degradates? 

<bullet≤ Have States seen an increase 

or decrease in the number of PWSs 

impacted by metolachlor and/or its 

degradates? 

<bullet≤ How many systems have 

taken wells or sources offline due to 

impacts from metolachlor and/or its 

degradates? 

B. Methyl tertiary-butyl ether 

1. Background 

Methyl tertiary-butyl ether (MTBE) is 

a volatile organic compound 

synthesized for use as a gasoline 

additive. First used as an octane 

enhancer to improve engine 

performance, MTBE is also used to 

reduce emissions that form carbon 

monoxide and ozone. Leaking 

underground storage tanks, gasoline 

distribution facilities, and even 

recreational boating can release MTBE 

into the environment. 

In 1997, EPA issued a drinking water 

advisory of 20 to 40 [mu]g/L based on 

taste and odor (USEPA, 1997b). EPA is 

currently revising its health risk 

assessment for MTBE, and thus, will not 

be making a regulatory determination 

for MTBE as part of this action. The IRIS 

Chemical Assessment Tracking System 

http://cfpub.epa.gov/iristrac/index.cfm 

has the most up-to-date information on 


rmajette on DSK29S0YB1PROD with MISCELLANEOUS
24050 Federal Register / Vol. 72, No. 83 / Tuesday, May 1, 2007 / Proposed Rules 

the status of the MTBF health risk 

assessment and interested members of 

the public should check that Web site to 

find out the latest schedule. 

The Agency collected data on MTBE 

occurrence as part of the UCMR 1 

survey. In addition, EPA evaluated 

several sources of supplemental 

occurrence information described in the 

supporting documentation for this 

action entitled ‘‘Regulatory 

Determinations Support Document for 

Selected Contaminants from the Second 

Drinking Water Contaminant Candidate 

List (CCL 2)’’ (USEPA, 2006a). Section 

VI.B.2 provides a summary of some of 

the data and information on MTBE 

occurrence collected to date. 

2. Occurrence Information 

a. UCMR 1. EPA collected sampling 

results for MTBE from over 98.9 percent 

(3,068 of 3,100) of the large PWSs and 

over 99.5 percent (796 of 800) of the 

small systems required to sample under 

UCMR 1. Based on these data, 19 public 

water systems (0.49 percent of the 3,864 

sampled) in 14 states (CA, CT, GA, IL, 

MA, MO, NH, NJ, NM, NY, PA, SD, TN, 

and WV) reported MTBE occurrence in 

drinking water. These 19 systems 

reported MTBE in 26 samples at the 

minimum reporting level of 5 [mu]g/L 

or above, representing approximately 

0.33 percent (or 754 thousand of 226 

million) of the population served by the 

public water systems that sampled for 

MTBE. (USEPA, 2006a) 

Of the PWSs reporting detections at or 

above 5 [mu]g/L (the MRL), 15 were 

ground water systems and 4 were 

surface water systems. One small 

ground water system (49 [mu]g/L) and 3 

large ground water PWSs (48 [mu]g/L, 

36 [mu]g/L, and 33.2 [mu]g/L) reported 

MTBE at levels greater than 20 [mu]g/ 

L (the lower end of the taste and odor 

threshold). One large surface water 

system (33 [mu]g/L) reported MTBE at 

levels greater than 20 [mu]g/L. The 

remaining 14 systems had detects 

between 5 [mu]g/L and 20 [mu]g/L 

(USEPA, 2006a). 

b. USGS studies/surveys/reviews. In 

2003, the USGS reported results of 

national source water sampling 

(previously introduced in section 

III.B.2.a.(2)). USGS sampling included a 

random study of a representative sample 

of untreated source waters (known as 

the ‘‘Random Survey’’) and a study of 

source waters from areas known or 

suspected of having MTBE (known as 

the ‘‘Focused Survey’’). In the Random 

Survey, USGS found that none of the 

source waters exceeded 20 [mu]g/L, and 

the three highest concentration sources 

ranged from 6 [mu]g/L to 19.5 [mu]g/L 

(Grady, 2003). Of the areas known or 

suspected of having MTBE in the 

Focused Survey, USGS found that 5 

percent (e.g., ground waters for 7 of the 

134 systems) had concentrations greater 

than 20 [mu]g/L (Delzer and Ivahnenko, 

2003a). 

USGS also reviewed the literature for 

national, regional, and State MTBE 

information (Delzer and Ivahnenko, 

2003b), including 13 state-wide 

assessments. This information is 

summarized in Table 6. USGS noted 

that because study objectives varied, 

information varied in terms of reporting 

levels, sampling frequencies, and 

sources (e.g., ambient water, public and 

homeowner wells, treated drinking 

water). 

Previously, USGS (Grady and Casey, 

2001) studied MTBE occurrence in the 

drinking water of 12 States (New 

England and the Mid-Atlantic). The 

study found less than 1 percent of the 

CWSs had drinking water samples at or 

above 20 [mu]g/L, while 7.8 percent of 

the CWSs had MTBE at 1 [mu]g/L or 

higher. 

BILLING CODE 6560–50–P 

BILLING CODE 6560–50–C 

c. New England Interstate Water 

Pollution Control Commission 

(NEIWPCC). In 2003, the NEIWPCC 

surveyed the States under a grant from 

EPA’s Office of Underground Storage 

Tanks (UST). Twenty-six States 

estimated that they had public wells 

that were contaminated by MTBE at 

some level, and of those, 5 States (ME, 


rmajette on DSK29S0YB1PROD with MISCELLANEOUSEP01MY07.055
Federal Register / Vol. 72, No. 83 / Tuesday, May 1, 2007 / Proposed Rules 24051 

NH, NJ, DE, and MD) estimated having 

detectable levels of MTBE in at least 100 

public water supply wells. Thirteen 

States did not know the answer, 8 States 

did not respond, and 3 States reported 

that no PWS wells were impacted. The 

survey established no reporting level to 

define ‘‘contamination.’’ Only 3 States 

documented the basis for their estimates 

(projected from several studies, raw and 

treated water analyses, and a survey of 

funded petroleum spill projects) 

(NEIWPCC, 2003). 

d. California Department of Health 

Services. In 2000, California developed 

a drinking water standard of 13 [mu]g/ 

L for MTBE (CA DHS, 2000). According 

to California’s annual compliance 

reports, there were no violations of the 

13 [mu]g/L standard by public water 

systems in 2002 and 2003, and 2 

violations at 2 public water systems 

(serving almost 14,000 people) in 2004 

(CA DHS, 2002; CA DHS, 2003; CA 

DHS, 2004). 

e. Other Sources of Data. In April 

2005, the Environmental Working 

Group (EWG, 2005) released a report, 

Like Oil and Water, on their Web page. 

In response to Freedom of Information 

Act requests, 29 State agencies 

submitted data to EWG. EPA informally 

evaluated the data posted by EWG to 

determine if this information might be 

useful in projecting state-wide 

occurrence. While EPA found the report 

interesting, the data as reported on the 

Web lacked some of the information 

needed to assess the representativeness 

and the quality of the data. For example, 

States submitted different time periods 

of monitoring data (e.g., Alaska 

submitted 7 months of data for 1 system 

during the 2000 timeframe and Illinois 

submitted data that spanned 1990 to 

2002). States did not report monitoring 

results for every system. Also, the data 

do not indicate if the samples came 

from source water or finished water, 

from ground water or surface water, the 

analytical method used for analysis nor 

the reporting level, the frequency of the 

sampling (e.g., annual, quarterly), 

number of samples from each water 

system, number of non-detects, etc. 

3. Request for Additional MTBE 

Occurrence Information 

As discussed earlier, EPA is not 

making a regulatory determination for 

MTBE; however, EPA is presenting this 

information because of ongoing interest 

in MTBE. And as noted earlier, 

additional information is presented in 

the regulatory support document for this 

action (i.e., USEPA, 2006a). While the 

Agency waits for the final health risk 

assessment, EPA will continue to collect 

and evaluate occurrence information. 

The Agency requests any data, 

information, or analyses that may be 

available on the following topics: 

<bullet≤ Are there additional 

occurrence data for MTBE in 

community and non-community public 

water systems on a state-wide or more 

local basis? As noted in the previous 

section, the State data submitted to 

EWG lack some elements needed to 

assess the quality of the data, as 

required in EPA’s guidance for 

information quality guidelines (USEPA, 

2003c), and project state-wide 

occurrence. 

<bullet≤ What analytical method and 

reporting limit were used to gather these 

data? 

<bullet≤ Has there been an increase or 

decrease in the number of impacted 

PWSs? Over what time frame? 

<bullet≤ For those PWSs whose water 

supplies have been impacted, has there 

been an increase or a decrease in the 

concentration of MTBE? 

<bullet≤ How many systems have 

taken wells or sources offline, 

consolidated with other PWSs, or added 

customers due to impacts from MTBE? 

<bullet≤ What treatments are being 

used in the field? What range of 

treatment effectiveness is being 

achieved? 

<bullet≤ Is the listing of State bans for 

MTBE shown in Table 7 complete? Have 

state-wide bans decreased MTBE 

contamination in drinking water? 

TABLE 7.—STATE ACTIONS BANNING MTBE (STATE-WIDE) 

[Adapted from USEPA, 2004g and McCarthy and Tiemann, 2005] 

State Effective date Extent of MTBE ban 

Arizona ................................................. January 1, 2005 ...................................................... 0.3% max volume in gasoline. 

California .............................................. December 31, 2003 ................................................ complete ban in gasoline. 

Colorado ............................................... April 30, 2002 .......................................................... complete ban in gasoline. 

Connecticut .......................................... January 1, 2004 ...................................................... complete ban in gasoline. 

Illinois ................................................... July 24, 2004 ........................................................... 0.5% max volume in gasoline. 

Indiana ................................................. July 24, 2004 ........................................................... 0.5% max volume in gasoline. 

Iowa ...................................................... July 1, 2000 ............................................................. 0.5% max volume in gasoline. 

Kansas ................................................. July 1, 2004 ............................................................. 0.5% max volume in gasoline. 

Kentucky .............................................. January 1, 2006 ...................................................... 0.5% max volume in gasoline. 

Maine ................................................... January 1, 2007 ...................................................... 0.5% max volume in gasoline. 

Michigan ............................................... June 1, 2003 ........................................................... complete ban in gasoline. 

Minnesota ............................................. July 2, 2005 ............................................................. complete ban in gasoline. (following partial ban in 

2000). 

Missouri ................................................ July 1, 2005 ............................................................. 0.5% max volume in gasoline. 

Montana ............................................... January 1, 2006 ...................................................... no more than trace amounts in gasoline. 

Nebraska .............................................. July 13, 2000 ........................................................... 1% max volume in gasoline. 

New Hampshire .................................... January 1, 2007 ...................................................... 0.5% max volume in gasoline. 

New Jersey .......................................... January 1, 2009 ...................................................... 0.5% max volume in gasoline. 

New York .............................................. January 1, 2004 ...................................................... complete ban in gasoline. 

North Carolina ...................................... January 1, 2008 ...................................................... 0.5% max volume in gasoline. 

Ohio ...................................................... July 1, 2005 ............................................................. 0.5% max volume in gasoline. 

Rhode Island ........................................ June 1, 2007 ........................................................... 0.5% max volume in gasoline. 

South Dakota ....................................... July 1, 2001 ............................................................. 0.5% max volume in gasoline. 

Vermont ................................................ January 1, 2007 ...................................................... 0.5% max volume in gasoline. 

Washington .......................................... January 1, 2004 ...................................................... 0.6% max volume in gasoline. 

Wisconsin ............................................. August 1, 2004 ........................................................ 0.5% max volume in gasoline. 


rmajette on DSK29S0YB1PROD with MISCELLANEOUS
24052 Federal Register / Vol. 72, No. 83 / Tuesday, May 1, 2007 / Proposed Rules 

27 Cyanobacteria are called blue-green algae even 

though they are technically bacteria. 

C. Microbial Contaminants 

1. Evaluation of Microbial 

Contaminants for Regulatory 

Determination. The 9 microbial 

contaminants listed on CCL 2 include: 

<bullet≤ Four virus groups— 

Caliciviruses, Echoviruses, 

Coxsackieviruses, and Adenoviruses 

<bullet≤ Four bacteria/bacterial 

groups-Aeromonas hydrophila; 

Helicobacter pylori; Mycobacterium 

avium intercellulare (or MAC); and 

Cyanobacteria (called blue-green 

algae27), fresh water algae, and the 

associated toxins 

<bullet≤ One group of protozoa— 

Microsporidia (Enterocytozoon bieneusi 

and Septata intestinalis, now renamed 

Encephalitozoon intestinalis). 

In addition to considering if the 

Agency had sufficient information to 

address the three statutory criteria listed 

in section II.B.1 (i.e., adverse health 

effects, known/likely occurrence, and 

meaningful opportunity for health risk 

reduction), the Agency also considered 

whether sufficient information was 

available to determine whether current 

treatment requirements adequately 

controlled for any of the 9 microbial 

contaminants. After consideration of 

these factors, the Agency determined 

that none of the 9 microbial 

contaminants have sufficient 

information at this time to address the 

three statutory criteria to make a 

regulatory determination. Table 8 

identifies the specific areas for which 

information is insufficient. 

TABLE 8.—INFORMATION GAPS FOR THE MICROBIAL CONTAMINANTS

Health effects Treatment Analytical 

methods Occurrence 

Microsporidia .................................. Aeromonas ................................... Aeromonas ................................... Aeromonas. 

Some Cyanotoxins ......................... MAC .............................................. MAC .............................................. MAC. 

Adenoviruses ................................ Helicobacter .................................. Helicobacter. 

Caliciviruses .................................. Microsporidia ................................ Adenoviruses. 

Coxsackieviruses .......................... Some Cyanotoxins ....................... Caliciviruses. 

Echoviruses .................................. ....................................................... Coxsackieviruses. 

Microsporidia ................................ ....................................................... Echoviruses. 

Some Cyanotoxins ....................... ....................................................... Microsporidia. 

Helicobacter .................................. ....................................................... Some Cyanotoxins. 

2. Research and Other Ongoing 

Activities. EPA has supported an active 

research program to fill the information 

gaps on the CCL 2 microorganisms. 

While several examples of the ongoing 

research activities are listed below, 

further information on these and other 

projects can be found on EPA’s Drinking 

Water Research Information Network 

(DRINK). DRINK is a publiclyaccessible, Web-based system that tracks 

over 1,000 ongoing research projects 

and can be accessed at: http:// 

www.epa.gov/safewater/drink/ 

intro.html. 

a. Virus. For the CCL virus groups (or 

surrogates), the Agency has initiated 

treatment studies that simulate realistic 

conditions where viruses may be 

protected in aggregates. EPA also plans 

to conduct virus removal/inactivation 

studies in drinking water treatment 

plants and/or pilot plants. In order to 

assess the effectiveness of treatment and 

to perform monitoring studies, methods 

development for viruses is also in 

progress. 

b. Bacteria. For Aeromonas spp., EPA 

recently completed a one-year UCMR 1 

survey of 293 public water systems. The 

Agency is currently attempting to 

characterize and distinguish pathogenic 

from non-pathogenic strains, as well as 

develop methods to detect Aeromonas 

virulence factors. For H. pylori, the 

Agency is in the process of developing 

a culture method and method for its 

identification. For MAC, preliminary 

drinking water surveys have been 

conducted using a culture method 

followed by genetic detection. EPA is 

also conducting further research into 

methods development and the 

characterization of virulence factors for 

this organism. 

EPA has funded projects to evaluate 

the effect of disinfectants on 

cyanotoxins, and on the removal of algal 

cells and cyanotoxins in a pilot scale 

treatment plant. EPA is developing 

analytical methods for potential use for 

future monitoring and has available 

analytical chemistry standards for the 

toxins of most concern in the United 

States—microcystin, 

cylindrospermopsin, and anatoxin-a. 

EPA has conducted several small-scale 

preliminary occurrence surveys for 

cyanotoxins using a screening method 

followed by confirmation by 

instrumental analysis. A number of 

health effects studies are also in 

progress on several high priority 

cyanotoxins. These include behavioral 

studies in mice, acute and subacute 

effects in neonatal mice, and biomarkers 

of human exposure. Risk assessments 

are being conducted at EPA on the 

cyanotoxins to determine reference 

doses where possible. The Agency has 

organized and participated in several 

workshops on cyanotoxins to assess the 

state-of-the-science. 

As an interim measure to assist public 

water utilities, the Agency is planning 

to develop an information sheet that 

discusses pertinent information on 

cyanobacteria and some of its key 

toxins. The document will discuss the 

state of the knowledge on the 

prevention and treatment of 

cyanobacteria and its toxins, as well as 

the available information on the 

potential health effects of some of the 

toxins. EPA requests comment from the 

public as to whether such a document 

would be useful for public water 

utilities. 

c. Protozoa. EPA has several ongoing 

projects to evaluate the susceptibility of 

microsporidia to chlorine and 

chloramine disinfectants. EPA has 

sponsored methods-related projects for 

microsporidia, which have included the 

use of fluorescent gene probes, real-time 

PCR, concentration methods, and 

immunomagnetic separation. Ongoing 

monitoring at EPA has revealed that 

microsporidia are present in ground 

water. EPA has funded work to 

determine exposure to microsporidia, 

and to determine strains (animal and 

human) of Enterocytozoon bieneusi 

found in water. EPA also held a 

workshop in 2003 on microsporidia to 

assess the state-of-the-science. 

VII. EPA’s Next Steps 

EPA intends to respond to the public 

comments it receives on the 11 


rmajette on DSK29S0YB1PROD with MISCELLANEOUS
Federal Register / Vol. 72, No. 83 / Tuesday, May 1, 2007 / Proposed Rules 24053 

28 The statute authorizes a nine-month extension 

of this promulgation date. 

preliminary determinations and 

subsequently issue its final regulatory 

determinations. Although the 

preliminary determinations for all 11 

contaminants are not to regulate, if after 

consideration of public comments, the 

Agency determines that a national 

primary drinking water regulation is 

warranted for any of these 11 

contaminants, the regulation would 

then need to be formally proposed 

within 24 months of the determination 

and promulgated 18 months following 

the proposal.28

VIII. References 

Agency for Toxic Substances and Disease 

Registry (ATSDR). 1992. Toxicological Profile 

for Boron. Atlanta, GA: Agency for Toxic 

Substances and Disease Registry, Public 

Health Service, U.S. Department of Health 

and Human Services. Available on the 

Internet at: http://www.atsdr.cdc.gov/ 

toxprofiles/tp26.html. 

ATSDR. 1996. Toxicological Profile for 

1,1,2,2-Tetrachloroethane. Available on the 

Internet at: http://www.atsdr.cdc.gov/ 

toxprofiles/tp93.html. 

ATSDR. 1998. Toxicological Profile for 2,4- 

and 2,6-Dinitrotoluene. Available on the 

Internet at: http://www.atsdr.cdc.gov/ 

toxprofiles/tp109.html. 

ATSDR. 2002. Toxicological Profile DDT, 

DDE, and DDD. Available on the Internet at: 

http://www.atsdr.cdc.gov/toxprofiles/ 

tp35.html. 

Allen, B.C., P.L. Strong, C.J. Price, S.A. 

Hubbard, and G.P. Datson. 1996. Benchmark 

Dose Analysis of Developmental Toxicity in 

Rats Exposed to Boric Acid. Fundamental 

and Applied Toxicology. Vol. 32. pp. 194– 

204. (As cited in USEPA, 2004b) 

Aribi, H., Y.J.C. Le Blanc, S. Antonsen, T. 

Sakuma. 2006. Analysis of Perchlorate in 

Foods and Beverages by Ion Chromatography 

Couple with Tandem Mass Spectrometry (IC– 

ESI–MS/MS). Analytica Chimica Acta. Vol. 

567, No. 1. pp. 39–47. 

Banerjee, B.M., D. Howard, and M.W. 

Woodard. 1968. Dyfonate (N–2790) safety 

evaluation by dietary administration to rats 

for 105 weeks. (As cited in USEPA, 1988b) 

Banerjee, B.D., A. Ray, and S.T. Pasha. 

1996. A Comparative Evaluation of 

Immunotoxicity of DDT and its Metabolites 

in Rats. Indian Journal of Experimental 

Biology. Vol. 34. pp. 517–522. (As cited in 

ATSDR, 2002) 

Barron, L., P.N. Nesterenko, and B. Paull. 

2006. Rapid On-line Preconcentration and 

Suppressed Micro-bore Ion Chromatography 

of Part per Trillion Levels of Perchlorate in 

Rainwater Samples. Analytica Chimica Acta. 

Vol. 567, No. 1. pp. 127–134. 

Blount, B.C., L. Valent[iacute]n-Blasini, 

D.L. Ashley. 2006a. Assessing Human 

Exposure to Perchlorate Using 

Biomonitoring. Journal of ASTM 

International. Vol. 3, No. 7. pp. 1–6. 

Blount, B.C., J.L. Pirkle, J.D. Osterloh, L. 

Valent[iacute]n-Blasini, and K.L. Caldwell. 

2006b. Urinary Perchlorate and Thyroid 

Hormone Levels in Adolescent and Adult 

Men and Women Living in the United States. 

Environmental Health Perspectives. Vol. 114, 

No. 12. pp. 1865–1871. 

Blount, B.C., L. Valent[iacute]n-Blasini, 

J.D. Osterloh, J.P. Mauldin, and J.L. Pirkle. 

2006c. Perchlorate Exposure of the U.S. 

Population, 2001–2002. Journal of Exposure 

Science and Environmental Epidemiology. 

Advance online publication 18 October 2006. 

Available on the Internet at: http:// 

www.nature.com/jes/journal/vaop/ncurrent/ 

pdf/7500535a.pdf. 

Blount, B.C., L. Valent[iacute]n-Blasini. 

2006. Analysis of Perchlorate, Thiocyanate, 

Nitrate and Iodide in Human Amniotic Fluid 

using Ion Chromatography and Electrospray 

Tandem Mass Spectrometry. Analytica 

Chimica Acta. Vol. 567, No. 1. pp. 87–93. 

CA DHS. 2000. California Department of 

Health Services. Final Statement of Reasons 

Primary MCL for MTBE. Title 22, California 

Code of Regulations. Available on the 

Internet at: http://www.dhs.ca.gov/ps/ 

ddwem/chemicals/mtbe/4–17– 

00MTBESOR.PDF. 

CA DHS. 2002. California Department of 

Health Services. Annual Compliance Report 

for Public Water Systems, Calendar Year 

2002. Available on the Internet at: http:// 

www.dhs.ca.gov/ps/ddwem/publications/ 

2002annualcompliancereport-final.pdf. 

CA DHS. 2003. California Department of 

Health Services. Annual Compliance Report 

for Public Water Systems, Calendar Year 

2003. Available on the Internet at: http:// 

www.dhs.ca.gov/ps/ddwem/publications/ 

2003ARCFinal.pdf. 

CA DHS. 2004. California Department of 

Health Services. Annual Compliance Report 

for Public Water Systems, Calendar Year 

2004. Available on the Internet at: http:// 

www.dhs.ca.gov/ps/ddwem/publications/ 

AnnualComplianceReport2004.pdf. 

CA DHS. 2006. California Department of 

Health Services. ‘‘Perchlorate in California 

Drinking Water: Monitoring Update.’’ 

Available on the Internet at: http:// 

www.dhs.ca.gov/ps/ddwem/chemicals/ 

perchl/monitoringupdate.htm. Updated June 

2, 2006. 

Caldwell K.L., Jones R., and Hollowell J.G. 

2005. Urinary iodine concentration: United 

States National Health And Nutrition 

Examination Survey 2001–2002. Thyroid. 

Vol. 15, pp. 692–699. 

Cockrell, K.O., M.W. Woodard, and G. 

Woodard. 1966. N–2790 Safety Evaluation by 

Repeated Oral Administration to Dogs for 14 

Weeks and to Rats for 13 Weeks. (As cited 

in USEPA, 1988b) 

Cortina, T. 1984. In vivo Bone Marrow 

Chromosome Study in Rats: Hι14,673. Final 

Report: Project No. 201–695. (As cited in 

USEPA, 1998e) 

Crawford-Brown, D., B. Raucher and M. 

Harrod, 2006. Intersubject Variability of Risk 

from Perchlorate in Community Water 

Supplies. Environmental Health 

Perspectives. 114(7): 975–79. 

Dasgupta, P.K., P.K. Martinelango, W.A. 

Jackson, T.A. Anderson, K. Tian, R.W. Tock, 

and S. Rajagopalan. 2005. The Origin of 

Naturally Occurring Perchlorate: The Role of 

Atmospheric Processes. Environmental 

Science and Technology. Vol. 39, No. 6. pp. 

1569–1575. 

Dasgupta, P.K., J.V. Dyke, A.B.Kirk, and 

A.W. Jackson. 2006. Perchlorate in the 

United States. Analysis of Relative Source 

Contributions to the Food Chain. 

Environmental Science and Technology. 

40(21):6608–6614. 

Delzer, G.C. and T. Ivahnenko. 2003a. 

Occurrence and Temporal Variability of 

Methyl tert-Butyl Ether (MTBE) and Other 

Volatile Organic Compounds in Select 

Sources of Drinking Water: Results of the 

Focused Survey. U.S. Geological Survey 

Water-Resources Investigations Report 02– 

4084, 65 p. Available on the Internet at: 

http://sd.water.usgs.gov/nawqa/pubs/wrir/ 

wrir02—4084.pdf. 

Delzer, G.C. and T. Ivahnenko. 2003b. A 

Review of Literature for Methyl tert-Butyl 

Ether (MTBE) in Sources of Drinking Water 

in the United States. U.S. Geological Survey 

Open-File Report 01–322, 16 p. Available on 

the Internet at: http://sd.water.usgs.gov/ 

nawqa/pubs/ofr/ofr01—322.pdf. 

Ellis, H.V., J.H. Hagensen, J.R. Hodgson, et 

al. 1979. Mammalian Toxicity of Munitions 

Compounds. Phase BI: Effects of Lifetime 

Exposure. Part I: 2,4-Dinitrotoluene. Final 

Report No. 7. (As cited in USEPA, 1992c) 

Ellis, H.V., C.B. Hong, C.C. Lee, J.C. Dacre, 

and J.P. Glennon. 1985. Subchronic and 

Chronic Toxicity Studies of 2,4- 

Dinitrotoluene. Part I: Beagle Dog. Journal of 

the American College of Toxicology. Vol. 4. 

pp. 233–242. (As cited in USEPA, 1992c) 

Ericksen, G.E. The Chilean nitrate deposits. 

American Scientist, 1983, 71, 366–374, and 

references cited therein, as cited in USEPA, 

2001c. 

EWG. 2005. Environmental Working 

Group. Like Oil and Water. http:// 

www.ewg.org/reports/oilandwater. 

Extoxnet. 1993. ‘‘Extension Toxicology 

Network Pesticide Information Profiles– 

Fonofos.’’ Available on the Internet at: http:// 

pmep.cce.cornell.edu/profiles/extoxnet/ 

dienochlor—glyphosate/fonofos—ext.html. 

Accessed March 10, 2006. 

Extoxnet. 1994. ‘‘Extension Toxicology 

Network Pesticide Information Profiles– 

Terbacil.’’ Available on the Internet at: http:// 

pmep.cce.cornell.edu/profiles/Extoxnet/ 

pyrethrins-ziram/terbacil-ext.html. Accessed 

March 10, 2006. 

Food and Drug Administration (FDA). 

2004. ‘‘Exploratory Data on Perchlorate in 

Food.’’ FDA Center for Food Safety and 

Applied Nutrition, Office of Plant & Dairy 

Foods. November 2004. Available on the 

Internet at: http://www.cfsan.fda.gov/dms/ 

clo4data.html 

Food and Drug Administration (FDA). 

2006. Center for Food Safety and Applied 

Nutrition, Office of Plant & Dairy Foods. 

Total Diet Study. Available on the Internet at: 

http://www.cfsan.fda.gov/comm/tds-toc.html. 

Field, E.A., C.J. Price, M.C. Marr, C.B. 

Myers, R.E. Morrissey, and B.A. Schwetz. 

1989. Final Report on the Developmental 

Toxicity of Boric Acid (CAS No. 10043–35– 

3) in CD–1-Swiss Mice. NTP Final Report No. 

89–250. (As cited in USEPA, 2004b) 

Frey, M.M., C. Seidel, M. Edwards, J. Parks, 

and L. McNeill. 2004. Occurrence Survey for 

Boron and Hexavalent Chromium. AwwaRF 

Report 91044F. 

Grady, S.J. 2003. A National Survey of 

Methyl tert-Butyl Ether and Other Volatile 


rmajette on DSK29S0YB1PROD with MISCELLANEOUS
24054 Federal Register / Vol. 72, No. 83 / Tuesday, May 1, 2007 / Proposed Rules 

Organic Compounds in Drinking-Water 

Sources: Results of the Random Survey. U.S. 

Geological Survey Water-Resources 

Investigations Report 02–4079, 85 p. 

Available on the Internet at: http:// 

sd.water.usgs.gov/nawqa/pubs/wrir/wrir02— 

4079.pdf. 

Grady, S.J. and G.D. Casey. 2001. 

Occurrence and Distribution of Methyl tertButyl Ether and Other Volatile Organic 

Compounds in Drinking Water in the 

Northeast and Mid-Atlantic Regions of the 

United States, 1993–98. U.S. Geological 

Survey Water-Resources Investigations 

Report 00–4228, 123 p. Available on the 

Internet at: http://sd.water.usgs.gov/nawqa/ 

pubs/wrir/wrir00.4228.pdf. 

Greer, M.A., G. Goodman, R.C. Pleuss, and 

S.E. Greer. 2002. Health Effect Assessment 

for Environmental Perchlorate 

Contamination: The Dose Response for 

Inhibition of Thyroidal Radioiodide Uptake 

in Humans. Environmental Health 

Perspectives. Vol. 110. pp. 927–937. 

Gruener, N. 1976. Ontogenetic 

Development of NADH-dependent 

Methemoglobin Reductase in Erythrocytes of 

Man and Rat. Journal of Toxicology and 

Environmental Health. Vol. 1. pp. 787–791. 

(As cited in ATSDR, 1998) 

Hamilton, P.A., T.L. Miller, and D.N. 

Myers. 2004. Water Quality in the Nation’s 

Streams and Aquifers: Overview of Selected 

Findings, 1991–2001. USGS Circular 1265. 

Available on the Internet at: http:// 

water.usgs.gov/pubs/circ/2004/1265/pdf/ 

circular1265.pdf 

Haskell Laboratories. 1965a. 14-Day Rat 

Feeding Study. (Unpublished study, as cited 

in USEPA, 1998e) 

Haskell Laboratories. 1965b. 3-Week Rabbit 

Dermal Toxicity Study. (Unpublished study, 

as cited in USEPA, 1998e) 

Haskell Laboratories. 1965c. Rat 90-day 

feeding study in Rats. (Unpublished study, as 

cited in USEPA, 1998e) 

Haskell Laboratories. 1980. Rat Oral 

Teratology with Terbacil. (Unpublished 

study, as cited in USEPA, 1998e) 

Haskell Laboratories. 1984. CHO (HGPRT) 

Gene Mutation Assay with Terbacil. 

(Unpublished study, as cited in USEPA, 

1998e) 

Hawley, G.G. 1981. Condensed Chemical 

Dictionary. 10th ed. New York, NY: Van 

Nostrand Reinhold Co. (As cited in ATSDR, 

1996) 

Hayes, W.J. 1982. Pesticides Studied in 

Man. Baltimore, MD: Williams and Wilkins. 

p. 413. (As cited in USEPA, 1988b) 

Hazardous Substances Database (HSDB). 

2004a. ‘‘TOXNET: Toxicology Data 

Network—Boron.’’ Available on the Internet 

at: http://toxnet.nlm.nih.gov/cgi-bin/sis/ 

search. [Search for boron.] Accessed 

November 1, 2004. 

HSDB. 2004b. ‘‘TOXNET: Toxicology Data 

Network—2,4-Dinitrotoluene.’’ Available on 

the Internet at:-http://toxnet.nlm.nih.gov/cgibin/sis/search. [Search for 2,4- 

dinitrotoluene.] Accessed November 1, 2004. 

HSDB. 2004c. ‘‘TOXNET: Toxicology Data 

Network—2,6-Dinitrotoluene.’’ Available on 

the Internet at: http://toxnet.nlm.nih.gov/cgibin/sis/search. [Search for 2,6- 

dinitrotoluene.] Accessed November 1, 2004. 

HSDB. 2004d. ‘‘TOXNET: Toxicology Data 

Network—Fonofos.’’ Available on the 

Internet at: http://toxnet.nlm.nih.gov/cgi-bin/ 

sis/search. [Search for fonofos.] Accessed 

November 1, 2004. 

Heindel, J.J., C.J. Price, E.A. Field, M.C. 

Marr, C.B. Myers, R.E. Morrissey, and B.A. 

Schwetz. 1992. Developmental Toxicity of 

Boric Acid in Mice and Rats. Fundamental 

and Applied Toxicology. Vol. 18. pp. 266– 

277. (As cited in USEPA, 2004b) 

Heindel, J.J., C.J. Price, and B.A. Schwetz. 

1994. The Developmental Toxicity of Boric 

Acid in Mice, Rats and Rabbits. 

Environmental Health Perspectives 

Supplements. Vol. 102, No. S7. pp. 107–112. 

(As cited in USEPA, 2004b) 

Henry, J. 1986. Skin Sensitization Test of 

Terbacil (IND–732–53) in Guinea Pigs for 

EPA Pesticide Registration. Revised. Report 

No. 600–85: MR No. 4581–277. (As cited in 

USEPA, 1998e) 

Hodge, M. 1995. Fonofos: 1-Year Oral 

Toxicity Study in Dogs. Report Number CTL/ 

P/4499, Study Number PDO944. Zeneca 

Central Toxicology Lab. (As cited in USEPA, 

1996c) 

Hong, C.B., H.V. Ellis, C.C. Lee, H. Sprinz, 

J.C. Dacre, and J.P. Glennon. 1985. 

Subchronic and Chronic Toxicity Studies of 

2,4-Dinitrotoluene. Part III. CD–1 Mice. 

Journal of the American College of 

Toxicology. Vol. 4, No. 4. pp. 257–269. (As 

cited in ATSDR, 1998) 

Hood, D. 1966. 15-exposure Skin 

Absorption Studies with 3-Tert-Butyl-5- 

Chloro-6-Methyluracil. Report No. 33–66. (As 

cited in USEPA, 1998e) 

Horner, J. 1993. Fonofos: Subchronic 

Neurotoxicity Study in Rats. Lab Project 

Number: CTL/P/3879, PRO889. Zeneca 

Central Toxicology Lab. (As cited in USEPA, 

1996c) 

International Agency for Research on 

Cancer (IARC). 1979. 1,1,2,2- 

Tetrachloroethane. IACR Monographs on the 

Evaluation of the Carcinogenic Risk of 

Chemicals to Humans: Some Halogenated 

Hydrocarbons. Vol. 20. pp. 477–489. (As 

cited in ATSDR, 1996) 

Institute of Medicine (IOM). 2001. 

‘‘Boron.’’ Chapter in Dietary Reference 

Intakes for Vitamin A, Vitamin K, Arsenic, 

Boron, Chromium, Copper, Iodine, Iron, 

Manganese, Molybdenum, Nickel, Silicon, 

Vanadium and Zinc. Washington, DC: 

National Academy Press. pp. 510–521. 

ISK Biotech Corporation. 1993. MRID No. 

42731001, 42998401 HED No. 010513. 

(Unpublished study, as cited in USEPA, 

1994) 

Ivahnenko, T., S.J. Grady, and G.C. Delzer. 

2001. Design of a National Survey of Methyl 

tert-Butyl Ether and Other Volatile Organic 

Compounds in Drinking-Water Sources. U.S. 

Geological Survey Open-File Report 01–271, 

42 p. Available on the Internet at: http:// 

sd.water.usgs.gov/nawqa/pubs/ofr/ofr01— 

271.pdf. 

Iyengar, G.V., W.B. Clarke, R.G. Downing, 

and J.T. Tanner. 1988. Lithium in Biological 

and Dietary Materials. Chapter in 

Proceedings of the 5th International 

Workshop on Trace Element Analytical 

Chemistry in Medicine and Biology. Vol. 5. 

pp. 267–269. (As cited in USEPA, 2004c) 

Jackson, W.A., P. Joseph, P. Laxman, K. 

Tan, P.N. Smith, L. Yu, and T.A. Anderson. 

2005. Perchlorate Accumulation in Forage 

and Edible Vegetation. Journal of 

Agricultural and Food Chemistry. Vol. 53, 

No. 2. pp. 369–373. 

Jackson W.A., K. Rainwater, T. Anderson, 

T. Lehman, R. Tock, S. Rajagopalan, and M. 

Ridley, 2004. Distribution and Potential 

Sources of Perchlorate in the High Plains 

Region of Texas. Texas Tech University 

Water Resources Center. 

Jeney, E., F. Bartha, L. Kondor, and S. 

Szendrei. 1957. Prevention of Industrial 

Tetrachloroethane Intoxication—Part III. 

Egeszsegtudomany. Vol. 1. pp. 155–164. (As 

cited in USEPA, 1989) 

Kang, N., T.A. Anderson, and W.A. 

Jackson. 2006. Photochemical Formation of 

Perchlorate from Aqueous Oxychlorine 

Anions. Analytica Chimica Acta. Vol. 567, 

No. 1. pp. 48–56. 

Kelce, W.R., C.R. Stone, S.C. Laws, L.E. 

Gray, J.A. Kemppainen and E.M. Wilson. 

1995. Persistent DDT Metabolite p,p’-DDE is 

a Potent Androgen Receptor Antagonist. 

Nature. Vol. 375. pp. 581–585. (As cited in 

ATSDR, 2002) 

Kirk, A.B., E.E. Smith, K. Tian, T.A. 

Anderson, and P.K. Dasgupta. 2003. 

Perchlorate in Milk. Environmental Science 

and Technology. Vol. 37, No. 21. pp. 4979– 

4981. 

Kirk, A.B., P.K. Martinelango, K. Tian, A. 

Dutta, E.E. Smith, and P.K. Dasgupta. 2005. 

Perchlorate and Iodide in Dairy and Breast 

Milk. Environmental Science and 

Technology. Vol. 39, No. 7. pp. 2011–2017. 

Kirk, A.B., J.V. Dyke, C.F. Martin, and P.K. 

Dasgupta. 2006. Temporal Patterns in 

Perchlorate, Thiocyanate and Iodide 

Excretion in Human Milk. Environmental 

Health Perspectives Online. November 2006. 

In press. 

Klopman, G., D. Fercu, and H.S. 

Rosenkranz. 1996. The Carcinogenic 

Potential of Dacthal and its Metabolites. 

Environmental Toxicology and Chemistry. 

Vol. 15, No. 2. pp. 80–84. 

Kolpin, D.W. and J.D. Martin. 2003. 

‘‘Pesticides in Ground Water: Summary 

Statistics; Preliminary Results from Cycle I of 

the National Water Quality Assessment 

Program (NAWQA), 1992–2001.’’ Available 

on the Internet at: http://ca.water.usgs.gov/ 

pnsp/pestgw/Pest-GW—2001—Text.html. 

Accessed August 24, 2004. 

Konietzko, H. 1984. Chlorinated Ethanes: 

Sources, Distribution, Environmental Impact, 

and Health Effects. Hazard Assessment of 

Chemicals Current Developments. Vol. 3. pp. 

401–448. (As cited in ATSDR, 1996) 

Lee, C.C., J.V. Dilley, J.R. Hodgson, D.O. 

Helton, W.J. Wiegand, D.N. Roberts, B.S. 

Andersen, B.N. Halfpap, L.D. Kurtz, and N. 

West. 1975. Mammalian Toxicity of Munition 

Compounds: Phase I. Acute Oral Toxicity, 

Primary Skin and Eye Irritation, Dermal 

Sensitization, and Disposition and 

Metabolism. (Unpublished study, as cited in 

ATSDR, 1998) 

Lee C.C., H.V. Ellis III, J.J. Kowalski, J.R. 

Hodgsen, R.D. Short, J.C. Bhandari, T.W. 

Reddig, and J.L. Minor. 1976. Mammalian 

Toxicity of Munitions Compounds. Phase II: 

Effects of Multiple Doses. Part III: 2,6- 


rmajette on DSK29S0YB1PROD with MISCELLANEOUS
Federal Register / Vol. 72, No. 83 / Tuesday, May 1, 2007 / Proposed Rules 24055 

Dinitrotoluene. (Unpublished study, as cited 

in USEPA, 1992c) 

Lee, C.C., H.V. Ellis III, J.J. Kowalski, J.R. 

Hodgson, and S.W. Hwang. 1978. 

Mammalian Toxicity of Munitions 

Compounds. Phase II: Effects of Multiple 

Doses. Part II: 2,4-Dinitrotoluene. 

(Unpublished study, as cited in ATSDR, 

1998) 

Lee, C.C., C.B. Hong, H.V. Ellis III, J.C. 

Dacre, and J.P. Glennon. 1985. Subchronic 

and Chronic Toxicity Studies of 2,4- 

Dinitrotoluene. Part II. CD Rats. Journal of the 

American College of Toxicology. Vol. 4. pp. 

243–256. (As cited in ATSDR, 1998) 

Lehman, K.B. and L. Schmidt-Kehl. 1936. 

Study of the 13 Most Important 

Chlorohydrocarbons from the Standpoint of 

Industrial Hygienics. Archiv Fuer Hygiene 

und Bakteriologie. Vol. 116. pp. 132–268. (As 

cited in ATSDR, 1996 and USEPA, 1989) 

Lobo-Mendonca, R. 1963. 

Tetrachloroethane—A Survey. British Journal 

of Industrial Medicine. Vol. 20. pp. 51–56. 

(As cited in ATSDR, 1996 and USEPA, 1989) 

Lomax, L.G., W.T. Stott, K.A. Johnson, L.L. 

Calhoun, B.L. Yano, and J.F. Quast. 1989. 

The Chronic Toxicity and Oncogenicity of 

Inhaled Technical Grade 1,3- 

Dichloropropene in Rats and Mice. 

Fundamental and Applied Toxicology. Vol. 

12. pp. 418–431. (As cited in USEPA, 2000a) 

Lopes, T.J. and S.G. Dionne. 1998. A 

Review of Semivolatile and Volatile Organic 

Compounds in Highway Runoff and Urban 

Stormwater. U.S. Geological Survey OpenFile Report 98–409, 67 p. Available on the 

Internet at: http://sd.water.usgs.gov/nawqa/ 

pubs/ofr/ofr98–409.pdf. 

Mackenzie, K. 1986. Two-generation 

Reproduction Study with EPTC in Rats: 

Report: Study No. 6100–108. Unpublished 

study prepared by Hazleton Laboratories 

America, Inc. 1192 p. (As cited in USEPA, 

1999c) 

Mage, D.T., R. Allen, G. Gondy, W. Smith, 

D.B. Barr, and L.L. Needham. 2004. 

Estimating Pesticide Dose from Urinary 

Pesticide Concentration Data by Creatinine 

Correction in the Third National Health and 

Nutrition Examination Survey (NHANES-III). 

Journal of Exposure Analysis and 

Environmental Epidemiology. Vol. 14. pp. 

457–465. 

Massachusetts Department of 

Environmental Protection (MA DEP). 2005. 

The Occurrence and Sources of Perchlorate 

in Massachusetts. Draft Report. Available on 

the Internet at: http://www.mass.gov/dep/ 

cleanup/sites/percsour.pdf. 

Massachusetts Department of 

Environmental Protection (MA DEP). 2006. 

Press Release. Massachusetts’ First-In-TheNation Perchlorate Standards Take Effect 

Today Drinking Water, Cleanup Standards of 

2 ppb Are Set to Protect Public Health. July 

28, 2006. 

Available on the Internet at: http:// 

www.mass.gov/dep/public/press/ 

pchl0706.htm. 

Malek, D. 1993. Combined Chronic 

Toxicity/Oncogenicity Study with DPXD732–66 (Terbacil) Two Year Feeding Study 

in Rats. Lab Project Number: 9027–001: 453– 

93: 18260. (As cited in USEPA, 1998e) 

Martin, J.D., C.G. Crawford, and S.J. 

Larson. 2003. ‘‘Pesticides in Streams: 

Summary Statistics; Preliminary Results from 

Cycle I of the National Water Quality 

Assessment Program (NAWQA), 1992–2001.’’ 

Available on the Internet at: http:// 

ca.water.usgs.gov/pnsp/pestsw/Pest-SW— 

2001—Text.html. Accessed August 24, 2004. 

Martinelango, P.K., K. Tian, and P.K. 

Dasgupta. 2006a. Perchlorate in Seawater: 

Bioconcentration of Iodide and Perchlorate 

by Various Seaweed Species. Analytica 

Chimica Acta. Vol. 567, No. 1. pp. 100–107. 

Martinelango, P.K., G. G[uuml]m[uuml]s, 

and P.K. Dasgupta. 2006b. Matrix 

Interference Free Determination of 

Perchlorate in Urine by Ion Association-Ion 

Chromatography-Mass Spectrometry. 

Analytica Chimica Acta. Vol. 567, No. 1. pp. 

79–86. 

McCarthy, J.E. and M. Tiemann. 2005. 

MTBE in Gasoline: Clean Air and Drinking 

Water Issues. CRS Report for Congress. 

Updated August 17, 2005. Available on the 

Internet at: http://www.cnie.org/nle/ 

crsreports/05aug/RL32787.pdf. 

Merrill, E.A., R.A. Clewell, P.J. Robinson, 

A.M. Jarabek, J.M. Gearhart, T.R. Sterner, and 

J.W. Fisher. 2005. PBPK Model for 

Radioactive Iodide and Perchlorate Kinetics 

and Perchlorate-Induced Inhibition of Iodide 

Uptake in Humans. Toxicological Sciences. 

Vol. 83. pp. 25–43. 

Miller, J.L., L. Sandvik, G.L. Sprague, A.A. 

Bickford, and T.R. Castles. 1979. Evaluation 

of Delayed Neurotoxic Potential of 

Chronically Administered Dyfonate in Adult 

Hens. Abstract presented in Toxicology and 

Applied Pharmacology. 48(Part 2):A197. 

Miller, J. 1987. Neurotoxicity of 90-day 

Oral Administration of Technical Dyfonate to 

Adult Hens. T–6237: Final Report. Stauffer 

Chemical Co. pp. 59. (As cited in USEPA, 

1996c) 

Minor, J., J. Downs, G. Zwicker, et al. 1982. 

A Teratology Study in CD–1 Mice with 

Dyfonate Technical. T–10192. Final Report. 

Stauffer Chemical Co. (As cited in USEPA, 

1988b) 

Minot, G.R. and L.W. Smith. 1921. The 

Blood in Tetrachlorethane Poisoning. 

Archives of Internal Medicine. Vol. 28. pp. 

687–702. (As cited in ATSDR, 1996) 

National Center for Food and Agricultural 

Policy (NCFAP). 2004. National Pesticide Use 

Database. [Searches for 1,3–DCP and 

FONOFOS]. Available on the Internet at: 

http://www.ncfap.org/database/national/ 

default.asp. Accessed August 24, 2004. 

National Cancer Institute (NCI). 1978. 

Bioassay of 1,1,2,2-Tetrachloroethane for 

Possible Carcinogenicity. NCI–CG–TR–27. 

(As cited in ATSDR, 1996) 

National Toxicology Program (NTP). 1985. 

Toxicology and Carcinogenesis Studies of 

Telone II (Technical Grade 1,3- 

Dichloropropene Containing 1% 

Epichlorohydrin as a Stabilizer) in F344/N 

Rats and B6C3F1 Mice (Gavage Studies). (As 

cited in USEPA, 2000a) 

National Research Council (NRC). 2005. 

Health Implications of Perchlorate Ingestion. 

National Academies Press, Board on 

Environmental Studies and Toxicology. 

January 2005. 276 p. 

NEIWPCC. 2003. The Compiled Results of 

the Survey of State Experiences with MtBE 

and Other Oxygenate Contamination at LUST 

Sites (March-April 2003): A Project of the 

New England Interstate Water Pollution 

Control Commission (NEIWPCC). Available 

on the Internet at: http://www.neiwpcc.org/ 

PDF—Docs/2003mtbecom.pdf. 

NTP. 1991a. Range Finding Studies: 

Developmental Toxicity—1,1,2,2- 

Tetrachloroethane When Administered via 

Feed in CD Sprague-Dawley Rats. NTP–91- 

RF/DT–017. 

NTP. 1991b. Range Finding Studies: 

Developmental Toxicity—1,1,2,2- 

Tetrachloroethane (Repeat) When 

Administered via Feed in Swiss CD–1 Mice. 

NTP–91-RF/DT–020. 

NTP. 2004. NTP Technical Report on the 

Toxicity Studies of 1,1,2,2-Tetrachloroethane 

Administered in Microcapsules in Feed to F– 

344/N Rats and B6C3F1 Mice. NIH 

Publication No. 04–4414. 

Orris, G.J., G.J. Harvey, D.T. Tsui, and J.E. 

Eldrige. 2003. Preliminary Analyses for 

Perchlorate in Selected Natural Materials and 

their Derivative Products. USGS Open-File 

Report 03–314. 

Pavkov, K. and D. Taylor. 1988. Rat 

Chronic Toxicity and Oncogenicity Study 

with Dyfonate. Laboratory Project ID T– 

11997. (Unpublished study, as cited in 

USEPA, 1996c) 

Pena Gonzalez, P., J. Perez-Rendon 

Gonzalez, E. Dominguez Alberdi, M. Gomez 

Labat, and J. Bajo Arenas. 1996. Epidemic 

Outbreak of Acute Food Poisoning Caused by 

Pesticides [Article in Spanish]. Atencion 

Primaria. Vol. 17, No. 7. pp. 467–70. 

Phillips, P.J., G.R. Wall, E.M. Thurman, 

D.A. Eckhardt, and J. Vanhoesen. 1999a. 

Metolachlor and Its Metabolites in Tile Drain 

and Stream Runoff in the Canajoharie Creek 

Watershed. Environmental Science and 

Technology. 33(20):3531–3537. 

Phillips, P.J., D.A. Eckhardt, S.A. 

Terracciano, and L. Rosenmann. 1999b. 

Pesticides and their Metabolites in Wells of 

Suffolk County, New York, 1998. U.S. 

Geological Survey Water-Resources 

Investigations Report 99–4095, 12p. 

Available on the Internet at: http:// 

ny.water.usgs.gov/projects/nypesticides/ 

reports/WRI99–4095.pdf. 

Price, C.J., R.W. Tyl, T.A. Marks., L.L. 

Paschke, T.A. Ledoux and J.R. Reel. 1985. 

Teratologic Evaluation of Dinitrotoluene in 

the Fischer 344 Rat. Fundamental and 

Applied Toxicology. Vol. 5. pp. 948–961. (As 

cited in USEPA, 1992c) 

Price, C.J., E.A. Field, M.C. Marr, C.B. 

Myers, R.E. Morrissey, and B.A. Schwetz. 

1990. Developmental Toxicity of Boric Acid 

(CAS No. 10043–35–3) in Sprague Dawley 

Rats. NTP Report No. 90–105. (As cited in 

USEPA, 2004b) 

Price, C.J., M.C. Marr, and C.B. Myers. 

1994. Determination of the No-ObservableAdverse-Effect Level (NOAEL) for 

Developmental Toxicity in Sprague-Dawley 

(CD) Rats Exposed to Boric Acid in Feed on 

Gestational Days 0 to 20, and Evaluation of 

Postnatal Recovery through Postnatal Day 21. 

Final Report. (As cited in USEPA, 2004b) 

Price, C.J., P.L. Strong, M.C. Marr, C.B. 

Myers, and F.J. Murray. 1996. Developmental 

Toxicity NOAEL and Postnatal Recovery in 

Rats Fed Boric Acid During Gestation. 

Fundamental and Applied Toxicology. Vol. 

32. pp. 179–193. (As cited in USEPA, 2004b) 


rmajette on DSK29S0YB1PROD with MISCELLANEOUS
24056 Federal Register / Vol. 72, No. 83 / Tuesday, May 1, 2007 / Proposed Rules 

Pulsford, A. 1991. First Amendment to a 

Teratology Study in CD–1 Mice with 

Dyfonate Technical (MRID No. 118423), Lab 

Project No. T–10l92, T–10192C. MRID No. 

42057601. (Unpublished study as cited in 

USEPA, 1996c) 

Rajagopalan, S., T.A. Anderson, L. 

Fahlquist, K.A. Rainwater, M. Ridley, and 

W.A. Jackson. 2006. Widespread Presence of 

Naturally Occurring Perchlorate in High 

Plains of Texas and New Mexico. 

Environmental Science and Technology. Vol. 

40. pp. 3156–3162. 

Rheineck, B. and J. Postle. 2000. 

Chloroacetanilide Herbicide Metabolites in 

Wisconsin Groundwater. Wisconsin 

Department of Agriculture, Trade, and 

Consumer Protection. Available on the 

Internet at: http://datcp.state.wi.us/arm/ 

agriculture/land-water/water-quality/pdf/ 

metabrpt.pdf. 

Sanchez, C.A. 2004. Perchlorate Residues 

on Agricultural Produce Irrigated by Water 

from the Colorado River. Report Submitted to 

the USDA–ARS under a Cooperative 

Agreement. 

Sanchez, C.A., R.I Krieger, N. Khandaker, 

R.C. Moore, K.C. Holts, and L.L. Neidel. 

2005a. Accumulation and Perchlorate 

Exposure Potential of Lettuce Produced in 

the Lower Colorado River Region. Journal of 

Agricultural and Food Chemistry. Vol. 53. 

pp. 5479–5486. 

Sanchez C.A., K.S. Crump, R.I. Krieger, 

N.R. Khandaker, and J.P. Gibbs. 2005b. 

Perchlorate and Nitrate in Leafy Vegetables of 

North America. Environmental Science and 

Technology. Vol. 39, No. 24, pp 9391–9397. 

Sanchez C.A., R.I. Krieger, N.R. Khandaker, 

L. Valentin-Blasini, and B.C. Blount. 2006. 

Potential Perchlorate Exposure from Citrus 

sp. Irrigated with Contaminated Water. 

Analytica Chimica Acta. Vol. 567, No. 1. pp. 

33–38. 

Sauerhoff, M. 1987. A Teratology Study in 

Rabbits with Dyfonate Technical. T-l2630: 

Volume 1: Final Report: Laboratory Project 

ID: WIL 27027. (As cited in USEPA, 1996c) 

Schilt, A.A. Perchloric Acid and 

Perchlorates. GFS Chemicals, Inc.: Columbus, 

OH, 1979, p. 35, and references therein, as 

cited in USEPA, 2001c. 

Schmidt P., S. Binnevies, R. Gohlke, and R. 

Roth. 1972. Subacute Action of Low 

Concentration of Chlorinated Ethanes on Rats 

with and without Additional Ethanol 

Treatment. I. Biochemical and 

Toxicometrical Aspects, Especially Results in 

Subacute and Chronic Toxicity Studies with 

1,1,2,2-Tetrachloroethane. Internationales 

Archiv Fur Arbeitsmedizin. Vol. 30. pp. 283– 

298. 

Seidel, C. 2006. Email Communication to 

Brent Ranalli at The Cadmus Group, Inc. 

[concerning boron data from an AWWARFsponsored study, with data in an attached 

spreadsheet]. Denver, CO: McGuire Malcolm 

Pirnie; May 19, 2006. 

Snyder, S.A., R.C. Pleus, B.J. Vanderford, 

and J.C. Holady. 2006. Perchlorate and 

Chlorate in Dietary Supplements and Flavor 

Enhancing Ingredients. Analytica Chimica 

Acta. Vol. 567, No. 1. pp. 26–32. 

Solomon, H. 1984. Embryo-Fetal Toxicity 

and Teratogenicity Study of Terbacil by 

Gavage in the Rabbit. Medical Research 

Project No. 4512–001: Haskell Report No. 

528–83. (As cited in USEPA, 1998e) Sprague, 

G. and G. Zwicker. 1987. 18-Month Dietary 

Oncogenicity Study with Dyfonate Technical 

in Mice. Final Report: T–11995. (As cited in 

USEPA, 1996c) 

Stott, W.T., K.A. Johnson, T.K. Jeffries, K.T. 

Haut, and S.N. Shabrang. 1995. Telone II Soil 

Fumigant: Two-year Chronic Toxicity/ 

Oncogenicity Study in Fischer 344 Rats. 

Study ι M–003993–031l. (As cited in USEPA, 

2000a) 

T[eacute]llez, R.T., P.M. Chac[oacute]n, 

C.R. Abraca, B.C. Blount, C.B. Van 

Landingham, K.S. Crump, and J.P. Gibbs. 

2005. Chronic Environmental Exposure to 

Perchlorate Through Drinking Water and 

Thyroid Function During Pregnancy and the 

Neonatal Period. Thyroid. Vol. 15, No. 9. pp. 

963–975. 

Thelin, G.P. and L.P. Gianessi. 2000. 

Method for Estimating Pesticide Use for 

County Areas of the Conterminous United 

States. U.S. Geological Survey Open-File 

Report 00–250, 62 p. Available on the 

Internet at: http://ca.water.usgs.gov/pnsp/ 

rep/ofr00250/ofr00250.pdf. 

USEPA. 1986. EPA Guidelines for 

Carcinogen Risk Assessment. Federal 

Register. Vol. 51, No. 185. p. 33992, 

September 24, 1986. 

USEPA. 1987. Substitution of 

Contaminants and Priority List of Additional 

Substances Which May Require Regulation 

Under the Safe Drinking Water Act. Federal 

Register. Vol. 52, No. 130. p. 25720, July 8, 

1987. 

USEPA. 1988a. ‘‘Integrated Risk 

Information System (IRIS), p,p’’- 

Dichlorodiphenyldichloroethylene (DDE).’’ 

August 1988. Available on the Internet at: 

http://www.epa.gov/iris/subst/0328.htm. 

Accessed February 2, 2005. 

USEPA. 1988b. Fonofos Health Advisory. 

EPA Report 820–K–88–003. August, 1988. 

USEPA. 1989. 1,1,2,2-Tetrachloroethane 

Health Advisory. May, 1989. 

USEPA. 1990a. National Pesticide Survey: 

Survey Analytes. EPA Report 570–9–90– 

NPS2. Available on the Internet at: http:// 

nepis.epa.gov/pubtitleOSWER.htm. [Search 

for document number 570990NPS2.] 

USEPA. 1990b. National Survey of 

Pesticides in Drinking Water Wells. Phase I 

Report. EPA Report 570–9–90–015. 

USEPA. 1990c. ‘‘Integrated Risk 

Information System (IRIS), 2,4-/2,6- 

Dinitrotoluene Mixture.’’ September 1990. 

Available on the Internet at: http:// 

www.epa.gov/iris/subst/0397.htm. Accessed 

December 16, 2004. 

USEPA. 1990d. ‘‘Integrated Risk 

Information System (IRIS), S-Ethyl 

Dipropylthiocarbamate (EPTC).’’ September 

1990. Available on the Internet at: http:// 

www.epa.gov/iris/subst/0237.htm. Accessed 

February 2, 2005. 

USEPA. 1991. ‘‘Integrated Risk Information 

System (IRIS), Fonofos.’’ March 1991. 

Available on the Internet at: http:// 

www.epa.gov/iris/subst/0158.htm. Accessed 

February 2, 2005. 

USEPA. 1992a. National Primary Drinking 

Water Regulation—Synthetic Organic 

Chemicals and Inorganic Chemicals; National 

Primary Drinking Water Regulations 

Implementation. Federal Register. Vol. 57, 

No. 138. p. 31776, July 17, 1992. 

USEPA. 1992b. Pesticides in Ground Water 

Database: A Compilation of Monitoring 

Studies, 1971–1991. National Summary. 

Office of Prevention, Pesticides and Toxic 

Substances. EPA Report 734–12–92–001. 

Available on the Internet at: http:// 

nepis.epa.gov/pubtitleOPPTS.htm. [Search 

for document number 7341292001.] 

USEPA. 1992c. 2,4-& 2,6-Dinitrotoluene 

(DNT) Health Advisory. EPA Report 820–R– 

92–002. April 1992. 

USEPA. 1994. ‘‘Integrated Risk Information 

System (IRIS), Dacthal.’’ August 1994. 

Available on the Internet at: http:// 

www.epa.gov/iris/subst/0221.htm. Accessed 

February 2, 2005. 

USEPA. 1995. Reregistration Eligibility 

Decision (RED)—Metolachlor. EPA Report 

738–R–95–006. Washington, DC: USEPA 

Office of Prevention, Pesticides and Toxic 

Substances. April 1995. Available on the 

Internet at: http://www.epa.gov/oppsrrd1/ 

REDs/0001.pdf. 

USEPA. 1996a. Proposed Guidelines for 

Carcinogen Risk Assessment. Federal 

Register. Vol. 61, No. 79. p. 17960, April 23, 

1996. 

USEPA. 1996b. ‘‘Integrated Risk 

Information System (IRIS), p,p’- 

Dichlorodiphenyltrichloroethane (DDT).’’ 

February 1996. Available on the Internet at: 

http://www.epa.gov/iris/subst/0147.htm. 

Accessed February 2, 2005. 

USEPA. 1996c. Memorandum—041701. 

Fonofos (Dyfonate[supreg]). Draft Toxicology 

Chapter for Reregistration Eligibility. Health 

Effects Division. September 11, 1996. 

USEPA. 1997a. Announcement of the Draft 

Drinking Water Contaminant Candidate List; 

Notice. Federal Register. Vol. 62, No. 193. p. 

52193, October 6, 1997. 

USEPA. 1997b. Drinking Water Advisory: 

Consumer Acceptability Advice and Health 

Effects Analysis on Methyl Tertiary-Butyl 

Ether (MTBE). EPA Report 822-F–97–009. 

December 1997. Available on the Internet at: 

http://www.epa.gov/waterscience/drinking/ 

mtbefact.pdf. 

USEPA. 1998a. Announcement of the Draft 

Drinking Water Contaminant Candidate List; 

Notice. Federal Register. Vol. 63, No. 40. p. 

10273, March 2, 1998. 

USEPA. 1998b. Reregistration Eligibility 

Decision (RED)—1,3-Dichloropropene. EPA 

Report 738-R–98–016. Washington, DC: 

Office of Prevention, Pesticides and Toxic 

Substances. December 1998. Available on the 

Internet at: http://www.epa.gov/oppsrrd1/ 

REDs/0328red.pdf. 

USEPA. 1998c. Reregistration Eligibility 

Decision (RED)—DCPA. EPA Report 738–R– 

98–005. Washington, DC: Office of 

Prevention, Pesticides and Toxic Substances. 

November 1998. Available on the Internet at: 

http://www.epa.gov/oppsrrd1/REDs/ 

0270red.pdf. 

USEPA. 1998d. Notice of Receipt of 

Requests to Voluntarily Cancel Certain 

Pesticide Registrations. Federal Register. Vol. 

63, No. 87. p. 25033, May 6, 1998. 

USEPA. 1998e. Reregistration Eligibility 

Decision (RED)—Terbacil. EPA Report 738– 

R–97–011. Washington, DC: Office of 

Prevention, Pesticides and Toxic Substances. 

January 1998. Available on the Internet at: 

http://www.epa.gov/oppsrrd1/REDs/ 

0039red.pdf. 


rmajette on DSK29S0YB1PROD with MISCELLANEOUS
Federal Register / Vol. 72, No. 83 / Tuesday, May 1, 2007 / Proposed Rules 24057 

USEPA. 1999a. Guidelines for Carcinogen 

Risk Assessment. NCEA–F–0644, Review 

Draft. July 1999. Available on the Internet at: 

http://www.epa.gov/iris/cancer—gls.pdf. 

USEPA. 1999b. Revisions to the 

Unregulated Contaminant Monitoring 

Regulation for Public Water Systems. Federal 

Register. Vol. 64, No. 180. p. 50556, 

September 17, 1999. 

USEPA. 1999c. Reregistration Eligibility 

Decision (RED)—EPTC. EPA Report 738–R– 

99–006. Washington, DC: Office of 

Prevention, Pesticides and Toxic Substances. 

December 1999. Available on the Internet at: 

http://www.epa.gov/oppsrrd1/REDs/ 

0064red.pdf. 

USEPA. 1999d. Reregistration Eligibility 

Decision (RED) Facts—O-Ethyl S-phenyl 

ethylphosphonodithiolate (Fonofos). EPA 

Report 738–F–99–019. Washington, DC: 

Office of Prevention, Pesticides and Toxic 

Substances. November 1999. Available on the 

Internet at: http://www.epa.gov/oppsrrd1/ 

REDs/factsheets/0105fact.pdf. 

USEPA. 2000a. ‘‘Integrated Risk 

Information Systems (IRIS), 1,3- 

Dichloropropene.’’ May 2000. Available on 

the Internet at: http://www.epa.gov/iris/ 

subst/0224.htm. Accessed February 2, 2005. 

USEPA. 2000b. Unregulated Contaminant 

Monitoring Regulation for Public Water 

Systems: Analytical Methods for Perchlorate 

and Acetochlor; Announcement of 

Laboratory Approval and Performance 

Testing (PT) Program for the Analysis of 

Perchlorate; Final Rule and Proposed Rule. 

Federal Register. Vol. 65, No. 42. p. 11372, 

March 2, 2000. 

USEPA. 2001a. Notice of Opportunity to 

Provide Additional Information and 

Comment on Draft Revised Guidelines for 

Carcinogen Risk Assessment (July 1999), 

Availability of Draft Revised Guidelines, and 

Adoption of Draft Revised Guidelines as 

Interim Guidance. Federal Register. Vol. 66, 

No. 230. p. 59593, November 29, 2001. 

USEPA. 2001b. Unregulated Contaminant 

Monitoring Regulation for Public Water 

Systems; Analytical Methods for List 2 

Contaminants; Clarifications to the 

Unregulated Contaminant Monitoring 

Regulation. Federal Register. Vol. 66, No. 8. 

p. 2273, January 11, 2001. 

USEPA. 2001c. Survey of Fertilizers and 

Related Materials for Perchlorate (ClO4). EPA 

Report 600–R–01–049. Cincinnati, OH: Office 

of Research and Development. July 2001. 

USEPA. 2002a. Announcement of 

Preliminary Regulatory Determinations for 

Priority Contaminants on the Drinking Water 

Contaminant Candidate List. Federal 

Register. Vol. 67, No. 106. p. 38222, June 3, 

2002. 

USEPA. 2002b. The Toxics Release 

Inventory (TRI) and Factors to Consider 

When Using TRI Data. EPA Report 260–F– 

02–017. November 2002. Available on the 

Internet at: http://www.epa.gov/triinter/ 

2002—tri—brochure.pdf. 

USEPA. 2003a. Announcement of 

Regulatory Determinations for Priority 

Contaminants on the Drinking Water 

Contaminant Candidate List. Federal 

Register. Vol. 68, No. 138. p. 42898, July 18, 

2003. 

USEPA. 2003b. How are the Toxics Release 

Inventory Data Used? EPA Report 260–R– 

002–004. May 2003. Available on the Internet 

at: http://www.epa.gov/tri/guide—docs/ 

2003—datausepaper.pdf. 

USEPA. 2003c. A summary of general 

assessment factors for evaluating the quality 

of scientific and technical information. EPA 

100/B–03/001, June 2003. Available on the 

Web at: http://www.epa.gov/OSA/spc/pdfs/ 

assess2.pdf. 

USEPA. 2004a. Drinking Water 

Contaminant Candidate List 2; Notice. 

Federal Register. Vol. 69, No. 64. p. 17406, 

April 2, 2004. 

USEPA. 2004b. Toxicological Review of 

Boron and Compounds. EPA Report 635–04– 

052. June 2004. Available online at: http:// 

www.epa.gov/iris/toxreviews/0410-tr.pdf. 

USEPA. 2004c. ‘‘Integrated Risk 

Information System (IRIS), Boron and 

Compounds.’’ August 2004. Available on the 

Internet at: http://www.epa.gov/iris/subst/ 

0410.htm. Accessed February 2, 2005. 

USEPA. 2004d. Memorandum—TPA 

(Tetrachloroterephthalic Acid)-Metabolite of 

DCPA (Dacthal). Evaluation of Potential for 

Carcinogenicity. Office of Prevention, 

Pesticide, and Toxic Substances. May 25, 

2004. 

USEPA. 2004e. Memorandum—EFED 

Review of a Telone Well Monitoring Study. 

Office of Prevention, Pesticide, and Toxic 

Substances. March 10, 2004. 

USEPA. 2004f. Email Communication 

between James Breithaupt and Wynne Miller 

regarding the Memorandum—EFED Review 

of a Telone Well Monitoring Study. 

September 8, 2004. 

USEPA. 2004g. State Actions Banning 

MTBE (State-wide). EPA Report 420–B–04– 

009. June 2004. Available on the Internet at: 

http://www.epa.gov/mtbe/420b04009.pdf. 

USEPA. 2005a. Notice—Drinking Water 

Contaminant Candidate List 2; Final Notice. 

Federal Register. Vol. 70, No. 36. p. 9071, 

February 24, 2005. 

USEPA. 2005b. Guidelines for Carcinogen 

Risk Assessment. EPA Report 630–P–03– 

001B. March 2005. Available on the Internet 

at: http://www.epa.gov/ttn/atw/cancer— 

guidelines—final—3–25–05.pdf. 

USEPA. 2005c. Supplemental Guidance for 

Assessing Susceptibility to Early-life 

Exposure to Carcinogens. EPA Report 630–R– 

03–003F. March 2005. Available on the 

Internet at: http://www.epa.gov/ttn/atw/ 

childrens—supplement—final.pdf. 

USEPA. 2005d. Application of New Cancer 

Guidelines. Memorandum from Acting 

Administrator Stephen L. Johnson. March 29, 

2005. 

USEPA. 2005e. ‘‘Integrated Risk 

Information System (IRIS), Perchlorate and 

Perchlorate Salts.’’ February 2005. Available 

on the Internet at: http://www.epa.gov/iris/ 

subst/1007.htm. Accessed February 2, 2005. 

USEPA. 2005f. Notice—DCPA; Order to 

Amend to Terminate Uses. Federal Register. 

Vol. 70, No. 143. p. 43408, July 27, 2005. 

USEPA. 2005g. Unregulated Contaminant 

Monitoring Regulation (UCMR) for Public 

Water Systems Revisions. Proposed Rule. 

Federal Register. Vol. 70, No. 161. p. 49093, 

August 22, 2005. 

USEPA. 2006a. Regulatory Determinations 

Support Document for Selected 

Contaminants from the Second Drinking 

Water Contaminant Candidate List (CCL 2). 

EPA Report 815–D–06–007. Draft. December 

2006. 

USEPA. 2006b. The Analysis of 

Occurrence Data from the First Unregulated 

Contaminant Monitoring Regulation (UCMR 

1) in Support of Regulatory Determinations 

for the Second Drinking Water Contaminant 

Candidate List. EPA Report 815–D–06–007. 

Draft. December 2006. 

USEPA. 2006c. The Analysis of Occurrence 

Data from the Unregulated Contaminant 

Monitoring (UCM) Program and National 

Inorganics and Radionuclides Survey (NIRS) 

in Support of Regulatory Determinations for 

the Second Drinking Water Contaminant 

Candidate List. EPA Report 815–D–06–009. 

Draft. December 2006. 

USEPA. 2006d. ‘‘TRI Explorer: Trends— 

Boron.’’ Last modified June 8, 2005. 

Available on the Internet at: http:// 

www.epa.gov/triexplorer/trends.htm. [Search 

for boron trichloride and boron trifluoride.] 

Accessed February 8, 2006. 

USEPA. 2006e. ‘‘TRI Explorer: Trends— 

1,3-Dichloropropylene.’’ Last modified June 

8, 2005. Available on the internet at: http:// 

www.epa.gov/triexplorer/trends.htm. [Search 

for 1,3-dichloropropylene.] Accessed 

February 8, 2006. 

USEPA. 2006f. ‘‘TRI Explorer: Trends—2,4- 

Dinitrotoluene and 2,6-Dinitrotoluene.’’ Last 

modified June 8, 2005. Available on the 

Internet at: http://www.epa.gov/triexplorer/ 

trends.htm. [Search for 2,4-dinitrotoluene, 

2,6-dinitrotoluene, and dinitrotoluene (mixed 

isomers).] Accessed February 8, 2006. 

USEPA. 2006g. ‘‘TRI Explorer: Trends— 

EPTC.’’ Last modified June 8, 2005. Available 

on the Internet at: http://www.epa.gov/ 

triexplorer/trends.htm. [Search for ethyl 

dipropylthiocarbamate.] Accessed February 

8, 2006. 

USEPA. 2006h. ‘‘TRI Explorer: Trends— 

Terbacil.’’ Last modified June 8, 2005. 

Available on the Internet at: http:// 

www.epa.gov/triexplorer/trends.htm. [Search 

for terbacil.] Accessed February 8, 2006. 

USEPA. 2006i. ‘‘TRI Explorer: Trends— 

1,1,2,2-Tetrachloroethane.’’ Last modified 

June 8, 2005. Available on the Internet at: 

http://www.epa.gov/triexplorer/trends.htm. 

[Search for 1,1,2,2-tetrachloroethane.] 

Accessed February 8, 2006. 

USEPA. 2006j. Health Effects Support 

Document for Boron. EPA Report 822–R–06– 

005. December 2006. 

USEPA. 2006k. Health Effects Support 

Document for Dacthal Degradates: 

Tetrachloroterephthalic Acid (TPA) and 

Monomethyl Tetrachloroterephthalic Acid 

(MTP). EPA Report 822–R–06–006. December 

2006. 

USEPA. 2006l. Health Effects Support 

Document for 1,1-Dichloro-2,2-bis(pchlorophenyl)ethylene (DDE). EPA Report 

822–R–06–0007. December 2006. 

USEPA. 2006m. Health Effects Support 

Document for S-Ethyl dipropylthiocarbamate 

(EPTC). EPA Report 822–R–06–008. 

December 2006. 

USEPA. 2006n. Health Effects Support 

Document for Fonofos. EPA Report 822–R– 

06–009. December 2006. 

USEPA. 2006o. Health Effects Support 

Document for Terbacil. EPA Report 822–R– 

06–010. December 2006. 


rmajette on DSK29S0YB1PROD with MISCELLANEOUS
24058 Federal Register / Vol. 72, No. 83 / Tuesday, May 1, 2007 / Proposed Rules 

USEPA. 2006p. Health Effects Support 

Document for 1,3-Dichloropropene. EPA 

Report 822–R–06–011. December 2006. 

USEPA. 2006q. Health Effects Support 

Document for 1,1,2,2-Tetrachloroethane. EPA 

Report 822–R–06–012. December 2006. 

USEPA. 2006r. Health Advisory for 2,4- 

and 2,6-Dinitrotoluene. EPA Report 822–R– 

06–017. December 2006. 

USGS. 2004. ‘‘Mineral Commodity 

Summaries, January 2004—Boron.’’ January 

2004. Available on the Internet at: http:// 

minerals.usgs.gov/minerals/pubs/ 

commodity/boron/boronmcs04.pdf. 

USGS. 2006. ‘‘Information Page on Karst 

Geology.’’ Last modified December 5, 2005. 

Available on the Internet at: http:// 

water.usgs.gov/ogw/karst/. Accessed 

February 20, 2006. 

Valent[iacute]n-Blasini, L., J.P. Mauldin, D. 

Maple, and B.C. Blount. 2005. Analysis of 

Perchlorate in Human Urine Using Ion 

Chromatography and Electrospray Tandem 

Mass Spectrometry. Analytical Chemistry. 

Vol. 77. pp. 2475–2481. 

Wang, H., A. Eaton, and B. Narloch. 2002. 

National Assessment of Perchlorate 

Contamination Occurrence. Denver: AWWA 

Research Foundation and American Water 

Works Association. 

Wazeter, F.X., R.H. Buller, and R.G. Geil. 

1964. Ninety-day Feeding Study in the Rat: 

IRDC No. 125–004. (Unpublished study, as 

cited in USEPA, 1998e) 

Wazeter, F.X., R.H. Buller, and R.G. Geil. 

1967a. Two-year Feeding Study in the Dog: 

IRDC No. 125–011. (Unpublished study, as 

cited in USEPA, 1998e) 

Wazeter, F.X., R.H. Buller, and R.G. Geil. 

1967b. Three-generation Reproduction Study 

in the Rat: IRDC No. 125–012. (Unpublished 

study, as cited in USEPA, 1998e) 

Woodard, M.W., C.L. Leigh, and G. 

Woodard. 1968. Dyfonate (N–2790) Threegeneration Reproduction Study in Rats. 

(Unpublished study, as cited in USEPA, 

1996c) 

Woodard, M.W., J. Donoso, and J.P. Gray, 

et al. 1969. Dyfonate (N–2790) Safety 

Evaluation by Dietary Administration to Dogs 

for 106 Weeks. (Unpublished study, as cited 

in USEPA, 1988b and USEPA, 1996c) 

World Health Organization (WHO), 1994. 

Indicators for Assessing Iodine Deficiency 

Disorders and Their Control through Salt 

iodization. WHO/NUT/94.6.Geneva:World 

Health Organization(WHO)/International 

Council for the Control of Iodine Deficiency 

Disorders (Unpublished study, as cited in 

Blount et al., 2006b) 

Dated: April 12, 2007. 

Stephen L. Johnson, 

Administrator. 

[FR Doc. E7–7539 Filed 4–30–07; 8:45 am] 

BILLING CODE 6560–50–P 


rmajette on DSK29S0YB1PROD with MISCELLANEOUS